ORIGINAL_ARTICLE
Mechanisms of spinal cord injury regeneration in zebrafish: a systematic review
Objective(s):To determine the molecular and cellular mechanisms of spinal cord regeneration in zebrafish. Materials and Methods: Medical databases of PubMed and Scopus were searched with following key words: Zebrafish; spinal cord injuries; regeneration; recovery of function. The map of mechanisms was performed using Xmind software. Results: Wnt/ß-catenin signaling, L1.1, L1.2, Major vault protein (MVP), contactin-2 and High mobility group box1 (HMGB1) had positive promoting effects on axonal re-growth while Ptena had an inhibitory effect. Neurogenesis is stimulated by Wnt/ß-catenin signaling as well as HMGB1, but inhibited by Notch signaling. Glial cells proliferate in response to fibroblast growth factor (fgf) signaling and Lysophosphatidic acid (LPA). Furthermore, fgf signaling pathway causes glia bridge formation in favor of axonal regeneration. LPA and HMGB1 in acute phase stimulate inflammatory responses around injury and suppress regeneration. LPA also induces microglia activation and neuronal death in addition to glia cell proliferation, but prevents neurite sprouting. Conclusion: This study provides a comprehensive review of the known molecules and mechanisms in the current literature involved in the spinal cord injury (SCI) regeneration in zebrafish, in a time course manner. A better understanding of the whole determining mechanisms for the SCI regeneration should be considered as a main goal for future studies.
https://ijbms.mums.ac.ir/article_9620_28aba05bea19f3bb3aeedbac3edd11bc.pdf
2017-12-01
1287
1296
10.22038/ijbms.2017.9620
Regeneration recovery of function
Spinal cord regeneration
Spinal cord injuries
Zebrafish
Zeynab
Noorimotlagh
zn.motlagh@yahoo.com
1
Medical Student, Iran University of Medical Sciences, Sina Trauma and Surgery Research Center, Tehran, Iran
AUTHOR
Mahla
Babaie
2
Medical Student, Iran University of Medical Sciences, Sina Trauma and Surgery Research Center, Tehran, Iran
AUTHOR
Mahdi
Safdarian
3
Iran University of Medical Sciences, Sina Trauma and Surgery Research Center, Tehran, Iran
AUTHOR
Tahereh
Ghadiri
4
Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Vafa
Rahimi-Movaghar
v_rahimi@sina.tums.ac.ir
5
Sina Trauma and Surgery Research Center, Tehran University of Medical Sciences, Tehran, 11365-3876, Iran
LEAD_AUTHOR
1. Pinto L, Gotz M. Radial glial cell heterogeneity--the source of diverse progeny in the CNS. Prog Neurobiol 2007; 83:2-23.
1
2. Rahimi-Movaghar V, Yazdi A, Karimi M, Mohammadi M, Firouzi M, Zanjani LO, et al. Effect of decompression on complete spinal cord injury in rats. International Journal of Neuroscience 2008; 118:1359-1373.
2
3. Rahimi-Movaghar V, Vaccaro AR, Mohammadi M. Efficacy of surgical decompression in regard to motor recovery in the setting of conus medullaris injury. J Spinal Cord Med 2006; 29:32-38.
3
4. Rahimi-Movaghar V, Saadat S, Vaccaro AR, Ghodsi SM, Samadian M, Sheykhmozaffari A, et al. The efficacy of surgical decompression before 24 hours versus 24 to 72 hours in patients with spinal cord injury from T1 to L1–with specific consideration on ethics: a randomized controlled trial. Trials 2009; 10:77.
4
5. Rahimi-Movaghar V, Sayyah MK, Akbari H, Khorramirouz R, Rasouli MR, Moradi-Lakeh M, et al. Epidemiology of traumatic spinal cord injury in developing countries: a systematic review. Neuroepidemiology 2013; 41:65-85.
5
6. Becker CG, Becker T. Zebrafish as a model system for successful spinal cord regeneration. Model organisms in spinal cord regeneration: John Wiley and Sons; 2007. 289-319.
6
7. Briona LK, Poulain FE, Mosimann C, Dorsky RI. Wnt/ß-catenin signaling is required for radial glial neurogenesis following spinal cord injury. Dev Biol 2015; 403:15-21.
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8. Becker T, Bernhardt RR, Reinhard E, Wullimann MF, Tongiorgi E, Schachner M. Readiness of zebrafish brain neurons to regenerate a spinal axon correlates with differential expression of specific cell recognition molecules. J Neurosci 1998; 18:5789-5803.
8
9. Briona LK, Poulain FE, Mosimann C, Dorsky RI. Wnt/ss-catenin signaling is required for radial glial neurogenesis following spinal cord injury. Dev Biol 2015; 403:15-21.
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10. Fleisch VC, Fraser B, Allison WT. Investigating regeneration and functional integration of CNS neurons: Lessons from zebrafish genetics and other fish species. Biochim Biophys Acta 2011; 1812:364-380.
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11. Wang Z, Reynolds A, Kirry A, Nienhaus C, Blackmore MG. Overexpression of Sox11 promotes corticospinal tract regeneration after spinal injury while interfering with functional recovery. J Neurosci 2015; 35:3139-3145.
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12. Yu YM, Cristofanilli M, Valiveti A, Ma L, Yoo M, Morellini F, et al. The extracellular matrix glycoprotein tenascin-C promotes locomotor recovery after spinal cord injury in adult zebrafish. Neuroscience 2011; 183:238-250.
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13. Panic N, Leoncini E, de Belvis G, Ricciardi W, Boccia S. Evaluation of the endorsement of the preferred reporting items for systematic reviews and meta-analysis (PRISMA) statement on the quality of published systematic review and meta-analyses. PLoS One 2013; 8:e83138.
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14. Hassannejad Z, Sharif-Alhoseini M, Shakouri-Motlagh A, Vahedi F, Zadegan SA, Mokhatab M, et al. Potential variables affecting the quality of animal studies regarding pathophysiology of traumatic spinal cord injuries. Spinal Cord 2015.
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15. Barreiro-Iglesias A, Mysiak KS, Scott AL, Reimer MM, Yang Y, Becker CG, et al. Serotonin promotes development and regeneration of spinal motor neurons in zebrafish. Cell Rep. 2015; 13:924-932.
15
16. Becker CG, Lieberoth BC, Morellini F, Feldner J, Becker T, Schachner M. L1.1 is involved in spinal cord regeneration in adult zebrafish. J Neurosci 2004; 24:7837-7842.
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17. Becker T, Becker CG. Regenerating descending axons preferentially reroute to the gray matter in the presence of a general macrophage/microglial reaction caudal to a spinal transection in adult zebrafish. J Comp Neurol 2001; 433:131-147.
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18. Bormann P, Roth LWA, Andel D, Ackermann M, Reinhard E. zfNLRR, a novel leucine-rich repeat protein is preferentially expressed during regeneration in zebrafish. Mol Cell Neurosci 1999; 13:167-179.
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19. Briona LK, Dorsky RI. Radial glial progenitors repair the zebrafish spinal cord following transection. Exp Neurol 2014; 256:81-92.
19
20. Chen T, Yu Y, Hu C, Schachner M. L1.2, the zebrafish paralog of L1.1 and ortholog of the mammalian cell adhesion molecule L1 contributes to spinal cord regeneration in adult zebrafish. Restor Neurol Neurosci 2016; 34:325-335.
20
21. Dias TB, Yang YJ, Ogai K, Becker T, Becker CG. Notch signaling controls generation of motor neurons in the lesioned spinal cord of adult zebrafish. J Neurosci 2012; 32:3245-3252.
21
22. Fang P, Pan HC, Lin SL, Zhang WQ, Rauvala H, Schachner M, et al. HMGB1 contributes to regeneration after spinal cord injury in adult zebrafish. Mol Neurobiol 2014; 49:472-483.
22
23. Goldshmit Y, Matteo R, Sztal T, Ellett F, Frisca F, Moreno K, et al. Blockage of lysophosphatidic acid signaling improves spinal cord injury outcomes. Am J Pathol 2012; 181:978-992.
23
24. Goldshmit Y, Sztal TE, Jusuf PR, Hall TE, Nguyen-Chi M, Currie PD. Fgf-dependent glial cell bridges facilitate spinal cord regeneration in zebrafish. J Neurosci 2012; 32:7477-7492.
24
25. Guo Y, Ma L, Cristofanilli M, Hart RP, Hao A, Schachner M. Transcription factor Sox11b is involved in spinal cord regeneration in adult zebrafish. Neuroscience 2011; 172:329-341.
25
26. Hui SP, Nag TC, Ghosh S. Characterization of proliferating neural progenitors after spinal cord injury in adult zebrafish. PLoS One 2015; 10:e0143595.
26
27. Hui SP, Dutta A, Ghosh S. Cellular response after crush injury in adult zebrafish spinal cord. Dev Dyn 2010; 239:2962-2979.
27
28. Kuscha V, Barreiro-Iglesias A, Becker CG, Becker T. Plasticity of tyrosine hydroxylase and serotonergic systems in the regenerating spinal cord of adult zebrafish. J Comp Neurol 2012; 520:933-951.
28
29. Kuscha V, Frazer SL, Dias TB, Hibi M, Becker T, Becker CG. Lesion-induced generation of interneuron cell types in specific dorsoventral domains in the spinal cord of adult zebrafish. J Comp Neurol 2012; 520:3604-3616.
29
30. Lin JF, Pan HC, Ma LP, Shen YQ, Schachner M. The cell neural adhesion molecule contactin-2 (TAG-1) is beneficial for functional recovery after spinal cord injury in adult zebrafish. PLoS One 2012; 7:e52376.
30
31. Liu D, Yu Y, Schachner M. Ptena, but not Ptenb, reduces regeneration after spinal cord injury in adult zebrafish. Exp Neurol 2014; 261:196-205.
31
32. Ma L, Shen YQ, Khatri HP, Schachner M. The asparaginyl endopeptidase legumain is essential for functional recovery after spinal cord injury in adult zebrafish. PLoS One 2014; 9:e95098.
32
33. Ma L, Yu YM, Guo Y, Hart RP, Schachner M. Cysteine- and glycine-rich protein 1a is involved in spinal cord regeneration in adult zebrafish. Eur J Neurosci 2012; 35:353-365.
33
34. Ogai K, Nakatani K, Hisano S, Sugitani K, Koriyama Y, Kato S. Function of Sox2 in ependymal cells of lesioned spinal cords in adult zebrafish. Neurosci Res 2014; 88:84-87.
34
35. Ogai K, Hisano S, Mawatari K, Sugitani K, Koriyama Y, Nakashima H, et al. Upregulation of anti-apoptotic factors in upper motor neurons after spinal cord injury in adult zebrafish. Neurochem Int 2012; 61:1202-1211.
35
36. Pan HC, Lin JF, Ma LP, Shen YQ, Schachner M. Major vault protein promotes locomotor recovery and regeneration after spinal cord injury in adult zebrafish. Eur J Neurosci 2013; 37:203-211.
36
37. Reimer MM, Kuscha V, Wyatt C, Sorensen I, Frank RE, Knuwer M, et al. Sonic hedgehog is a polarized signal for motor neuron regeneration in adult zebrafish. J Neurosci 2009; 29:15073-15082.
37
38. Reimer MM, Sorensen I, Kuscha V, Frank RE, Liu C, Becker CG, et al. Motor neuron regeneration in adult zebrafish. J Neurosci 2008; 28:8510-8516.
38
39. Schweitzer J, Gimnopoulos D, Lieberoth BC, Pogoda HM, Feldner J, Ebert A, et al. Contactin1a expression is associated with oligodendrocyte differentiation and axonal regeneration in the central nervous system of zebrafish. Mol Cell Neurosci 2007; 35:194-207.
39
40. Schweitzer J, Becker T, Becker CG, Schachner M. Expression of protein zero is increased in lesioned axon pathways in the central nervous system of adult zebrafish. GLIA 2003; 41:301-317.
40
41. Vajn K, Plunkett JA, Tapanes-Castillo A, Oudega M. Axonal regeneration after spinal cord injury in zebrafish and mammals: differences, similarities, translation. Neurosci Bull 2013; 29:402-410.
41
42. Yu Y, Schachner M. Syntenin-a promotes spinal cord regeneration following injury in adult zebrafish. Eur J Neurosci 2013; 38:2280-2289.
42
43. Yu YM, Gibbs KM, Davila J, Campbell N, Sung S, Todorova TI, et al. MicroRNA miR-133b is essential for functional recovery after spinal cord injury in adult zebrafish. Eur J Neurosci 2011; 33:1587-1597.
43
ORIGINAL_ARTICLE
Protective effect of metformin on toxicity of butyric acid and arsenic in isolated liver mitochondria and langerhans islets in male mice: an in vitro study
Objective(s): Arsenic, a toxic metal in drinking water and butyric acid (BA) is a free fatty acid found in many foods. These two can induce oxidative stress in some tissues. The present study investigated the protective effect of metformin against toxicity induced by Arsenic (As) and BA in isolated mice liver mitochondria and pancreatic islets. Materials and Methods: In this study, liver mitochondria were isolated by adopting different centrifugation methods and pancreatic islets isolated by a collagenase method. Mitochondria were incubated by BA (75 μM), As (100 μM) and metformin (0, 0.5, 1, 3, 10 mM) and the islets also incubated by BA (1000 μM), As (100 μM) and metformin (0, 1, 3, 10 mM) for 1 hr. At the end of study, mitochondrial viability (MTT), mitochondrial membrane potential (MMP), reactive oxygen species (ROS), malondial- dehyde (MDA), glutathione (GSH) and islets insulin secretion were measured employing specific relevant methods. Results: As and BA significantly increased ROS, MDA and ΔΨm levels and decreased GSH level, succinate dehydrogenase activity and insulin secretion. On the other hand, pretreatment with metformin, returned mitochondrial complex ІІ activity, reduced ROS, MDA and ΔΨm levels and increased GSH level and insulin secretion of pancreatic islets. Conclusion: As and BA in combination or in isolation induce oxidative stress in liver mitochondria and decrease insulin secretion of pancreatic islets. Metformin has a protective effect probably caused by its antioxidant feature. The findings suggest the potential role of metformin in mitochondria therapy and insulin secretion in many diseases.
https://ijbms.mums.ac.ir/article_9567_fd3146b6d49b8df8289a5023c15abecb.pdf
2017-12-01
1297
1305
10.22038/ijbms.2017.9567
Arsenic
Butyric acid
Islet insulin secretion
Liver mitochondrial
Metformin
Oxidative stress
Akram
Ahangarpour
mard-sa@ajums.ac.ir
1
Health Research Institute, Diabetes Research Center, Department of Physiology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
AUTHOR
Leila
zeidooni
leilazeidooni@gmail.com
2
Department of Toxicology, School of Pharmacy, Student Research Committee of Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
LEAD_AUTHOR
Mohsen
Rezaei
drmrezaei@hotmail.com
3
Department of pharmacology, School of Pharmacy, Tarbiat Modares University, Tehran, Iran
AUTHOR
Soheila
Alboghobeish
alboghobeish.s@ajums.ac.ir
4
Department of pharmacology, School of Pharmacy, Student Research Committee of Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
AUTHOR
Azin
samimi
5
Department of Toxicology, School of Pharmacy, Student Research Committee of Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
AUTHOR
Ali Akbar
Oroojan
aliakbar_oroojan@yahoo.com
6
Department of Physiology, Student Research Committee of Ahvaz Jundishapur University of Medical Science, Ahvaz, Iran
AUTHOR
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4. Dutta M, Ghosh D, Ghosh AK, Bose G, Chattopadhyay A, Rudra S, et al. High fat diet aggravates arsenic induced oxidative stress in rat heart and liver. Food Chem Toxicol 2014; 66:262-277.
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6. Kahya MC, Nazıroğlu M, Övey İS. Modulation of diabetes-induced oxidative stress, apoptosis, and Ca2+ entry through TRPM2 and TRPV1 channels in dorsal root ganglion and hippocampus of diabetic rats by melatonin and selenium. Mol Neurobiol 2017; 54:2345-2360.
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17. Mashayekhi V, Eskandari MR, Kobarfard F, Khajeamiri A, Hosseini MJ. Induction of mitochondrial permeability transition (MPT) pore opening and ROS formation as a mechanism for methamphetamine-induced mitochondrial toxicity. Naunyn Schmiedebergs Arch Pharmacol 2014; 387:47-58.
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18. Ahangarpour A, Oroojan AA, Rezaei M, Khodayar MJ, Alboghobeish S, Zeinvand M. Effects of butyric acid and arsenic on isolated liver mitochondria and pancreatic islets of male mouse. Gastroenterol Hepatol Bed Bench 2017; 10:44-53.
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19. Hickmann FH, Cecatto C, Kleemann D, Monteiro WO, Castilho RF, Amaral AU, et al. Uncoupling, metabolic inhibition and induction of mitochondrial permeability transition in rat liver mitochondria caused by the major long-chain hydroxyl monocarboxylic fatty acids accumulating in LCHAD deficiency. BBA Biomemb 2015; 1847:620-628.
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20. Hassani S, Yaghoubi H, Khosrokhavar R, Jafarian I, Mashayekhi V, Hosseini MJ, et al. Mechanistic view for toxic effects of arsenic on isolated rat kidney and brain mitochondria. Biologia 2015; 70:683-689.
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21. Mehrabadi AR, Jamshidzadeh A, Rashedinia M, Niknahad H. Study of the effects of ATP suppliers and thiol reductants on toxicity of pioglitazone in isolated rat liver mitochondria. Iran J Pharm Res 2015; 14:825-832.
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22. Keshtzar E, Khodayar M, Javadipour M, Ghaffari M, Bolduc D, Rezaei M. Ellagic acid protects against arsenic toxicity in isolated rat mitochondria possibly through the maintaining of complex II. Hum Exp Toxicol 2016; 35:1060-1072.
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23. Koliaki C, Szendroedi J, Kaul K, Jelenik T, Nowotny P, Jankowiak F, et al. Adaptation of hepatic mitochondrial function in humans with non-alcoholic fatty liver is lost in steatohepatitis. Cell Metab 2015; 21:739-746.
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45
ORIGINAL_ARTICLE
Curcumin enhances liver SIRT3 expression in the rat model of cirrhosis
Objective(s): Bill duct ligation (BDL) is a representative model of biliary cholestasis in animals. Curcumin has a protective effect on the liver; however, its underlying mechanisms are not completely known. This study explored the hepatoprotective activity of curcumin on hepatic damage via measuring the expression of sirtuin3 (SIRT3), AMP-activated protein kinase (AMPK), carnitine palmitoyltransferase 1A (CPT-1A), isocitrate dehydrogenase2 (IDH2) and manganese superoxide dismutase (MnSOD) as well as the level of serum lipid profile in the BDL fibrotic rat model. Materials and Methods: The study consisted of four groups (n=8 for each of Wistar rats): sham group, sham+curcumin (sham+Cur) group (received curcumin 100 mg/kg/day), BDL+Cur group, and BDL group. Transcription levels of SIRT3, AMPK, CPT-1A, IDH2, MnSOD and protein expression level of SIRT3 were measured by real-time PCR and Western blotting, respectively. Results: It was identified that SIRT3, AMPK, CPT-1A, IDH2 and MnSOD expression significantly decreased in BDL rats compared to sham rats; however, in the curcumin treatment of BDL rats, the expression of these factors increased significantly compared to BDL (P-value <0.05). It was, moreover, observed that treatment of BDL rats with curcumin reduced liver injury as verified by a reduction in the levels of total cholesterol (TC), triglyceride (TG), and low-density lipoprotein (LDL) and increase in high-density lipoprotein (HDL)(P-value <0.05). Conclusion: Curcumin reduced liver damage and oxidative stress in the liver tissue of BDL rats through up-regulation of SIRT3, AMPK, CPT-1A, IDH2 and MnSOD as well as changing the level of serum lipid profile.
https://ijbms.mums.ac.ir/article_9609_094dd2965d0edbc4239a34ddaf296a46.pdf
2017-12-01
1306
1311
10.22038/ijbms.2017.9609
Curcumin
Gene expression
Liver Cirrhosis
Rats
SIRT3 protein
Sara
Chenari
1
Department of Biochemistry, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran
AUTHOR
Fatemeh
Safari
fa.cardio@gmail.com
2
Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran
AUTHOR
Ali
Moradi
ralimoradi@gmail.com
3
Department of Biochemistry, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran
LEAD_AUTHOR
1.Teixeira C, Franco E, Oliveira PA, Colaco B, Gama A, Carrola J, et al. Effects of nebivolol on liver fibrosis induced by bile duct ligation in Wistar rats. In Vivo 2013; 27:635-640.
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2.Ji H, Jiang JY, Xu Z, Kroeger EA, Lee SS, Liu H, et al. Change in lipid profile and impairment of endothelium-dependent relaxation of blood vessels in rats after bile duct ligation. Life Sci 2003; 73:1253-1263.
2
3.Longo M, Crosignani A, Podda M. Hyperlipidemia in chronic cholestatic liver disease. Curr Treat Options Gastroenterol 2001; 4:111-114.
3
4.George J. Ascorbic acid concentrations in dimethylnitrosamine-induced hepatic fibrosis in rats. Clin Chim Acta 2003; 335:39-47.
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5.Bataller R, Brenner DA. Liver fibrosis. J Clin Invest 2005; 115:209-218.
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6.Halliwell B. Oxidative stress and cancer: have we moved forward? Biochem J 2007; 401:1-11.
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7.Aoyama T, Paik YH, Watanabe S, Laleu B, Gaggini F, Fioraso‐Cartier L, et al. Nicotinamide adenine dinucleotide phosphate oxidase in experimental liver fibrosis: GKT137831 as a novel potential therapeutic agent. Hepatology 2012; 56:2316-2327.
7
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20.Choudhury M, Jonscher KR, Friedman JE. Reduced mitochondrial function in obesity-associated fatty liver: SIRT3 takes on the fat. Aging (Albany NY) 2011; 3:175-178.
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25.Reyes-Gordillo K, Segovia J, Shibayama M, Tsutsumi V, Vergara P, Moreno MG, et al. Curcumin prevents and reverses cirrhosis induced by bile duct obstruction or CCl4 in rats: role of TGF-beta modulation and oxidative stress. Fundam Clin Pharmacol 2008; 22:417-427.
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40
ORIGINAL_ARTICLE
Genistein preserves the lungs of ovariectomized diabetic rats: addition to apoptotic and inflammatory markers in the lung
Objective(s): The role of isoflavones in pulmonary structure and function during menopause is not well studied. Moreover, the important role of estrogen in the physiological function of respiratory system has been revealed. Genistein, as an isoflavone, mimics estrogenic in diabetic and ovariectomized rats. Here, we hypothesized that genistein would reverse changes in the protein expression levels related to estrogen deficiency in the lung of ovariectomized diabetic rats. Materials and Methods: Wistar female rats were assigned to four experimental groups (n=10 in each group): sham, rats underwent laparotomy without removing the ovaries; OVX, rats that underwent ovariectomy; OVX.D, rats underwent bilateral ovariectomy and were fed a high-fat diet (HFD); OVX.D.G, ovariectomized diabetic rats with genistein administration (1 mg/kg /day). After ovariectomy, rats continued to feed HFD for a 4-week period. After 4 weeks of HFD feeding, a single dose of 30 mg/kg of streptozotocin was administered in the diabetic group. Genistein was administered for eight weeks. At the end of the experiment, lung tissue was removed and Western blotting technique and hematoxylin-eosin staining were used for evaluation of the lung. Results: Treatment with genistein significantly decreased inflammatory and apoptotic biomarkers in the ovariectomized diabetic rats compared to non-treated animals (P<0.05). Also, genistein exerted a protective effect in the lung architecture. Conclusion: Genistein partly reversed ovariectomy-induced changes in apoptotic and inflammatory biomarkers in the lung. Our data suggest that genistein treatment as a natural replacement therapy may prevent the estrogen deficiency effects in the lung of diabetic menopausal women.
https://ijbms.mums.ac.ir/article_9599_d56c4b094e1e1851c5aa1f4f4946f59a.pdf
2017-12-01
1312
1317
10.22038/ijbms.2017.9599
Apoptosis
Diabetes
Genistein
Inflammation
Ovariectomy
Faeze
Daghigh
f_daghigh@yahoo.com
1
Tuberculosis and Lung Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Alireza
Alihemmati
hemmati@yahoo.com
2
Department of Histology & Embryology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Pouran
Karimi
3
Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Parisa
Habibi
dr.habibi@yahoo.com
4
Department of Physiology, Hamadan University of Medical Sciences, Hamadan, Iran
AUTHOR
Naser
Ahmadiasl
n.ahmadiasl@gmail.com
5
Tuberculosis and Lung Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
LEAD_AUTHOR
1. Sandler M. Is the lung a'target organ'in Diabetes mellitus? Arch Intern Med 1990; 150:1385-1388.
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2. Goldman MD. Lung dysfunction in diabetes. Diabetes Care 2003; 26:1915-1918.
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3. van den Borst B, Gosker HR, Zeegers MP, Schols AM. Pulmonary function in diabetes: a metaanalysis. Chest 2010; 138:393-406.
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4. Wu J, Jin Z, Yan L-J. Redox imbalance and mitochondrial abnormalities in the diabetic lung. Redox Biol 2017; 11:51-59.
4
5. Dennis RJ, Maldonado D, Rojas MX, Aschner P, Rondón M, Charry L, et al. Inadequate glucose control in type 2 diabetes is associated with impaired lung function and systemic inflammation: a cross-sectional study. BMC Pulm Med 2010; 10:38.
5
6. Glassberg MK, Choi R, Manzoli V, Shahzeidi S, Rauschkolb P, Voswinckel R, et al. 17β-estradiol replacement reverses age-related lung disease in estrogen-deficient C57BL/6J mice. Endocrinology 2014; 155:441-448.
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7. Massaro D, Massaro GD. Estrogen regulates pulmonary alveolar formation, loss, and regeneration in mice. Am J Physiol Lung Cell Mol Physiol 2004; 287:L1154-L9.
7
8. Bitoska I, Krstevska B, Milenkovic T, Subeska-Stratrova S, Petrovski G, Mishevska SJ, et al. Effects of hormone replacement therapy on insulin resistance in postmenopausal diabetic women. Open Access Maced J Med Sci 2016; 4:83-88.
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9. Chen C-L, Weiss NS, Newcomb P, Barlow W, White E. Hormone replacement therapy in relation to breast cancer. Jama 2002; 287:734-741.
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10. Mosca L, Collins P, Herrington DM, Mendelsohn ME, Pasternak RC, Robertson RM, et al. Hormone replacement therapy and cardiovascular disease. Circulation 2001; 104:499-503.
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11. Serock MR, Wells AK, Khalil RA. Modulators of vascular sex hormone receptors and their effects in estrogen-deficiency states associated with menopause. Recent Pat Cardiovasc Drug Discov 2008; 3:165-86.
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12. Stephenson T, Setchell K, Kendall C, Jenkins D, Anderson J, Fanti P. Effect of soy protein-rich diet on renal function in young adults with insulin-dependent diabetes mellitus. Clin Nephrol 2005; 64: 1-11.
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13. Zhao L, Wang Y, Liu J, Wang K, Guo X, Ji B, et al. Protective effects of genistein and puerarin against chronic alcohol-induced liver injury in mice via antioxidant, anti-inflammatory, and anti-apoptotic mechanisms. J Agric Food Chem 2016; 64:7291-7297.
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14. Yousefi H, Alihemmati A, Karimi P, Alipour MR, Habibi P, Ahmadiasl N. Effect of genistein on expression of pancreatic SIRT1, inflammatory cytokines and histological changes in ovariectomized diabetic rat. Iran J Basic Med Sci 2017; 20:423-429.
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15. Irigoyen M-C, Paulini J, Flores LJ, Flues K, Bertagnolli M, Moreira ED, et al. Exercise training improves baroreflex sensitivity associated with oxidative stress reduction in ovariectomized rats. Hypertension 2005; 46:998-1003.
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16. Srinivasan K, Ramarao P. Animal models in type 2 diabetes research: an overview. Indian J Med Res 2007; 125:451-472.
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17. Su X, Meng X, Sun C, Liu L, Su B. Intramuscular injection of soluble receptor for advanced glycation endproducts expression vector prevents the development of streptozotocin‐induced diabetes mellitus in rats on high fat diet. J diabetes 2011; 3:309-316.
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18. Matori H, Umar S, Nadadur RD, Sharma S, Partow-Navid R, Afkhami M, et al. Genistein, a soy phytoestrogen, reverses severe pulmonary hypertension and prevents right heart failure in rats. Hypertension 2012; 60: 425-430.
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19. Faramoushi M, Sasan RA, Sarraf VS, Karimi P. Cardiac fibrosis and down regulation of GLUT4 in experimental diabetic cardiomyopathy are ameliorated by chronic exposures to intermittent altitude. JCVTR 2016; 8:26-33.
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20. Elfattah LIA. A comparative study between the effects of dietary soya and estrogen replacement therapy on the lung of ovariectomized albino rats: histological and immunohistochemical study. Egyptian Journal of Histology 2012; 35:34-42.
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21. Zhang X, Shan P, Sasidhar M, Chupp GL, Flavell RA, Choi AM, et al. Reactive oxygen species and extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase mediate hyperoxia-induced cell death in lung epithelium. Am J Respir Cell Mol Biol 2003; 28:305-315.
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22. Rayappa SP, Kowluru RA. Role of Raf-1 kinase in diabetes-induced accelerated apoptosis of retinal capillary cells. Int J Biomed Sci 2008; 4:20-28.
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23. Zhuang S, Yan Y, Daubert RA, Han J, Schnellmann RG. ERK promotes hydrogen peroxide-induced apoptosis through caspase 3 activation and inhibition of Akt in renal epithelial cells. Am J Physiol Renal Physiol 2007; 292:F440-F447.
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24. Tanaka Y, Nakayamada S, Fujimoto H, Okada Y, Umehara H, Kataoka T, et al. H-Ras/mitogen-activated protein kinase pathway inhibits integrin-mediated adhesion and induces apoptosis in osteoblasts. J Biol Chem 2002; 277:21446-21452.
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25. Guo J, Gu N, Chen J, Shi T, Zhou Y, Rong Y, et al. Neutralization of interleukin-1 beta attenuates silica-induced lung inflammation and fibrosis in C57BL/6 mice. Arch Toxicol 2013; 87:1963-1973.
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26. Falk R, Hacham M, Nyska A, Foley JF, Domb AJ, Polacheck I. Induction of interleukin-1β, tumour necrosis factor-α and apoptosis in mouse organs by amphotericin B is neutralized by conjugation with arabinogalactan. J Antimicrob Chemother 2005; 55:713-720.
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27. Gurjar MV, Deleon J, Sharma RV, Bhalla RC. Role of reactive oxygen species in IL-1β-stimulated sustained ERK activation and MMP-9 induction. Am J Physiol Heart Circ Physiol 2001; 281:H2568-H2574.
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28. Carmo A, Cunha-Vaz J, Carvalho A, Lopes M. L-arginine transport in retinas from streptozotocin diabetic rats: correlation with the level of IL-1β and NO synthase activity. Vision Res 1999; 39:3817-3823.
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29. Kim MJ, Lim Y. Protective effect of short-term genistein supplementation on the early stage in diabetes-induced renal damage. Mediators Inflamm 2013; 2013: 510212.
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30. Elmarakby AA, Ibrahim AS, Faulkner J, Mozaffari MS, Liou GI, Abdelsayed R. Tyrosine kinase inhibitor, genistein, reduces renal inflammation and injury in streptozotocin-induced diabetic mice. Vascul Pharmacol 2011; 55:149-156.
30
31. Zhong W-W, Liu Y, Li C-L. Mechanisms of genistein protection on pancreas cell damage in high glucose condition. Intern Med 2011; 50:2129-2134.
31
ORIGINAL_ARTICLE
Antimalarial and cytotoxic activities of roots and fruits fractions of Astrodaucus persicus extract
Objective(s):Astrodaucus persicus (Apiaceae) is one of the two species of this genus which grows in different parts of Iran. Roots of this plant were rich in benzodioxoles and used as food additive or salad in Iran and near countries. The aim of present study was evaluation of antimalarial and cytotoxic effects of different fractions of A. persicus fruits and roots extracts. Materials and Methods: Ripe fruits and roots of A. persicuswere extracted and fractionated by hexane, chloroform, ethyl acetate and methanol, separately. Antimalarial activities of fractions were performed based on Plasmodium berghei suppressive test in mice model and percentage of parasitemia and suppression were determined for each sample. Cytotoxicity of fruits and roots fractions were investigated against human breast adenocarcinoma (MCF-7), colorectal carcinoma (SW480) and normal (L929) cell lines by MTT assay and IC50 of them were measured. Results: Hexane fraction of roots extract (RHE) and ethyl acetate fraction of fruits extract (FEA) of A. persicus demonstrated highest parasite inhibition (73.3 and 72.3%, respectively at 500 mg/kg/day) which were significantly different from negative control group (P<0.05). In addition, RHE showed potent anticancer activities against MCF-7 (IC50 of 0.01 µg/ml), SW480 (IC50 of 0.36 µg/ml) and L929 (IC50 of 0.70 µg/ml) cell lines. Conclusion: According to the results, RHE and FEA fractions of A. persicus could be introduced as excellent choice for antimalarial drug discovery. In addition, cytotoxic activity of RHE was noticeable.
https://ijbms.mums.ac.ir/article_9554_a7e87ebddb3af00ab5b2be2c53f64369.pdf
2017-12-01
1318
1323
10.22038/ijbms.2017.9554
Antimalaria
Apiaceae
Astrodaucus persicus
Cytotoxic
MTT Assay
Plasmodium berghei
Saied
Goodarzi
saied.goodarzie@gmail.com
1
Medicinal Plants Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Mehdi
Nateghpour
nateghpourm@sina.tums.ac.ir
2
Department of Medical Parasitology and Mycology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Parina
Asgharian
parina.asgharian@gmail.com
3
Department of Pharmacognosy, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Abbas
Hadjiakhoondi
abbhadji@tums.ac.ir
4
Medicinal Plants Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Narguess
Yassa
yasa@tums.ac.ir
5
Medicinal Plants Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Saeed
Tavakoli
saeedtavakoli18@gmail.com
6
Department of Pharmacognosy, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Jalal
Mirzaei
jalalmrz123@gmail.com
7
Department of Pharmacognosy, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Leila
Farivar
nateghpourm@tums.ac.ir
8
Department of Medical Parasitology and Mycology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Afsaneh
Motevalli Haghi
a-motevalli@tums.ac.ir
9
Department of Medical Parasitology and Mycology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Zahra
Tofighi
ztofighi@tums.ac.ir
10
Medicinal Plants Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
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36. Capilla AS, Sanchez I, Caignard DH, Renard P, Pujol MD. Antitumor agents, Synthesis and biological evaluation of new compounds related to podophyllotoxin, containing the 2, 3-dihydro-1,4-benzodioxin system. Eur J Med Chem 2001;36:389-393.
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37. Chen GL, Yang L, Rowe TC, Halligan BD, Tewey K, Liu L. Non intercalative antitumor drugs interfere with the breakage-reunion reaction of mammalian DNA topoisomerase II. J Biol Chem1984; 259:13560-13566.
37
38. Hai-Hong W, Ke-Ming Q, Hong-En C, Yu-Shun Y, Yin L, Man X, et al. Synthesis, molecular docking and evaluation of thiazolyl-pyrazoline derivatives containing benzodioxole as potential anticancer agents. Bioorg Med Chem Lett 2013; 21:448-455
38
ORIGINAL_ARTICLE
Neuroprotection of a sesamin derivative, 1, 2-bis [(3-methoxy- phenyl) methyl] ethane-1, 2-dicaroxylic acid (MMEDA) against ischemic and hypoxic neuronal injury
Objective(s): Stroke may cause severe neuronal damage. The sesamin have been demonstrated to possess neuroprotection by its antioxidant and anti-inflammatory properties. One sesamin derivative was artificially composited, 1, 2-bis [(3-methoxyphenyl) methyl] ethane-1, 2-dicaroxylic acid (MMEDA) had been developed to study its antioxidative activity and neuroprotection. Materials and Methods: The infaction of Sprague Dawley (SD) rats and hypoxia models of BV-2 microglia or PC12 cells were investigated for in vivo and in vitro test respectively. Lipid peroxidation and reactive oxygen species (ROS), prostaglandin E2 (PGE2) and related signaling pathways from hypoxic cells were analyzed by ELISA or Western blot assay, respectively. Results: MMEDA showed a protective effect when given 90 min after the focal cerebral ischemia. The neuroprotection of MMEDA was further confirmed by attenuating ROS and PGE2 release from hypoxic BV-2 or PC12 cells. MMEDA significantly reduced hypoxia-induced JNK and caspase-3 (survival and apoptotic pathways) in PC12 cells. Conclusion: The neuroprotective effect of MMEDA on ischemia/hypoxia models was involved with its antioxidative activity and anti-inflammatory effects. These results suggest that MMEDA exert effective neuroprotection against ischemia/hypoxia injury.
https://ijbms.mums.ac.ir/article_9543_77daf6bcd5d378701cd069b724514d49.pdf
2017-12-01
1324
1330
10.22038/ijbms.2017.9543
Anti-inflammatory
Cerebral ischemia
Hypoxia
Neuroprotection
Reactive Oxygen Species
Sesamin derivative
Chang-Tsen
Hung
hongct@mail.ypu.edu.tw
1
Department of Health and Leisure Management, Yuanpei University of Medical Technology, Hsinchu, Taiwan
AUTHOR
Li-Dian
Chen
lidianchen87@yahoo.com
2
Department of Convalescence Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou China
AUTHOR
Chien-Wei
Hou
rolis.hou@mail.ypu.edu.tw
3
Department of Biotechnology and Pharmaceutical Technology, Yuanpei University of Medical Technology, Hsinchu, Taiwan
LEAD_AUTHOR
1. Ishida I, Kubo H, Suzuki S, Suzuki T, Akashi S, Inoue K, et al. Hypoxia diminishes toll-like receptor 4 expression through reactive oxygen species generated by mitochondria in endothelial cells. J Immunol 2002; 15:2069-2075.
1
2. Koga Y, Fujita M, Tsuruta R, Koda Y, Nakahara T, Yagi T, et al. Urinary trypsin inhibitor suppresses excessive superoxide anion radical generation in blood, oxidative stress, early inflammation, and endothelial injury in forebrain ischemia/reperfusion rats. Neurol Res 2010; 32:925-932.
2
3. Tsuruta R, Fujita M, Ono T, Koda Y, Koga Y, Yamamoto T, et al. Hyperglycemia enhances excessive superoxide anion radical generation, oxidative stress, early inflammation, and endothelial injury in forebrain ischemia/reperfusion rats. Brain Res 2010; 1309:155-163.
3
4. Hou CW, Wu CC, Yang CH, Jeng KC. Protective effects of sesamin and sesamolin on murine BV-2 microglia cell line under hypoxia. Neuroscience Letters 2004; 367:10–13.
4
5. Hou CW, Huang HM, Tzen JT, Jeng KC. Protective effects of sesamin and sesamolin on hypoxic neuronal and PC12 cells. J Neurosci Res 2003; 74:123-133.
5
6. Khan MM, Ishrat T, Ahmad A, Hoda MN, Khan MB, Khuwaja G, et al. Sesaminattenuates behavioral, biochemical and histological alterations induced by reversible middle cerebral artery occlusion in the rats. Chem Biol Interact. 2010; 183:255-263.
6
7. Bush ML, Miyashiro JS, Ingram VM. Activation of a neurofilament kinase, a tau kinase, and a tau phosphatase by decreased ATP levels in nerve growth factor-differentiated PC-12 cells. Proc Natl Acad Sci USA 1995; 92:1861-1865.
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8. Lu QR, Yuk D, Alberta JA, Zhu Z, Pawlitzky I, Chan J, et al. Sonic hedgehog--regulated oligodendrocyte lineage genes encoding bHLH proteins in the mammalian central nervous system. Neuron 2000; 25:317-329.
8
9. Chao CC, Hu S, Tsang M, Weatherbee J, Molitor TW, Anderson WR, et al. Effects of transforming growth factor-beta on murine astrocyte glutamine synthetase activity. Implications in neuronal injury. J Clin Invest 1992; 90:1786-1793.
9
10. Sun AY, Cheng JS. Neuroprotective effects of poly (ADP-ribose) polymerase inhibitors in transient focal cerebral ischemia of rats. Zhongguo Yao Li Xue Bao 1998; 19:104-108.
10
11. Hou RCW, Chen HL, Tzen JTC, Jeng KC. Effect of sesame antioxidants on LPS-induced NO production by BV2 microglial cells. Neuroreport 2003; 14:1815-1819.
11
12. Hou RCW, Chen YS, Chen CH, Chen YH, Jeng JC. Protective effect of 1,2,4-benzenetriol on LPS-induced NO production by BV2 microglial cells. J Biomed Sci 2006; 13:89–99.
12
13. Hamada N, Tanaka A, Fujita Y, Itoh T, Ono Y, Kitagawa Y, et al. Involvement of heme oxygenase-1 induction via Nrf2/ARE activation inprotectionagainst H2O2-induced PC12 cell death by a metabolite ofsesamincontained in sesame seeds. Bioorg Med Chem 2011; 19:1959-1965.
13
14. Barone FC, Irving EA, Ray AM, Lee JC, Kassis S, Kumar S, et al. a second-generation p38 mitogen-activated protein kinase inhibitor, reduces brain injury and neurological deficits in cerebral focal ischemia. J Pharmacol Exp Ther 2001; 296:312-321.
14
15. Kaminska B, Gozdz A, Zawadzka M, Ellert-Miklaszewska A, Lipko M. MAPK signal transduction underlying brain inflammation and gliosis as therapeutic target. Anat Rec(Hoboken) 2009; 292:1902-1913.
15
16. Zeng KW, Fu H, Liu GX, Wang XM. Icariin attenuates lipopolysaccharide-induced microglial activation and resultant death of neurons by inhibiting TAK1/IKK/NF-kappaB and JNK/p38 MAPK pathways. Int Immunopharmacol 2010; 10: 668-678.
16
17. Tabakman R, Jiang H, Levine RA, Kohen R, Lazarovici P. Apoptotic characteristics of cell death and the neuroprotective effect of homocarnosine on pheochromocytoma PC12 cells exposed to ischemia. J Neurosci Res 2004; 75: 499-507.
17
18. Ha SK, Moon E, Kim SY. Chrysin suppresses LPS-stimulated proinflammatory responses by blocking NF-κB and JNK activations in microglia cells. Neurosci Lett 2010; 485:143-147.
18
19. Liou SF, Hsu JH, Liang JC, Ke HJ, Chen IJ, Wu JR, et al. San-Huang-Xie-Xin-Tang protects cardiomyocytes against hypoxia/reoxygenation injury via inhibition of oxidative stress-induced apoptosis. J Nat Med 2012; 66:311-320.
19
20. Chiu PY, Chen N, Leong PK, Leung HY, Ko KM. Schisandrin B elicits a glutathione antioxidant response and protects against apoptosis via the redox-sensitive ERK/Nrf2 pathway in H9c2 cells. Mol Cell Biochem 2011; 350: 237-250.
20
21. Jamarkattel-Pandit N, Pandit NR, Kim MY, Park SH, Kim KS, Choi H, et al. Neuroprotective effect of defatted sesame seeds extract against in vitro and in vivo ischemicneuronal damage. Planta Med 2010; 76:20-26.
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22. Fujimura N, Sumita S, Narimatsu E. Alteration in diaphragmatic contractility during septic peritonitis in rats: effect of polyethylene glycol-absorbed superoxide dismutase. Crit Care Med 2000; 28:2406-2414.
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23. Shin MJ, Kim DW, Lee YP, Ahn EH, Jo HS, Kim DS, et al. Tat-glyoxalase protein inhibits against ischemic neuronal cell damage and ameliorates ischemic injury. Free Radic Biol Med 2013; 67C:195-210.
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24. Haddad JJ, Land SC. Redox/ROS regulation of lipopolysaccharide-induced mitogen-activated protein kinase (MAPK) activation and MAPK-mediated TNF-alpha biosynthesis. Br J Pharmacol 2002; 135:520-536.
24
ORIGINAL_ARTICLE
Effect of fetal and adult bovine serum on pyocyanin production in Pseudomonas aeruginosa isolated from clinical and soil samples
Objective(s): Pyocyanin is a blue-greenish redox-active pigment, produced by Pseudomonas aeruginosa, with a wide range of biological and biotechnological applications. Pyocyanin biosynthesis is regulated by the quorum-sensing (QS) system in which the expression of QS genes and QS-controlled virulence genes may be affected by serum as a complex medium. In the current study, effects of adult bovine serum (ABS) and fetal bovine serum (FBS) on the production of pyocyanin were examined in order to develop it. Materials and Methods: The presence of pyocyanin-producing specific genes and proteins in clinical and soil isolates of P. aeruginosa was confirmed using PCR and SDS-PAGE. Isolates were inoculated to media containing different concentrations of complement-active/-inactivated ABS or FBS and pyocyanin concentration was measured by spectrophotometry. Extracted pigment was characterized by using UV-Visible spectrophotometry. Titration of ABS antibodies against studied isolates was performed by the tube agglutination test. Results: Adding ABS to P. aeruginosa culture medium decreased pyocyanin production compared to the control, while its production increased in FBS-containing media (113.21±2.581 vs. 55.26±0.827 μg.ml-1 and 126.80±2.036 vs. 30.56±0.382 μg.ml-1 of C11 and E8 pyocyanin concentration in the presence of 10% FBS vs. control, respectively). Conclusion: In this study, due to the presence of inhibitors such as complement proteins and antibodies in ABS samples, the use of FBS devoid of antibodies was effective to increase pyocyanin production in studied isolates.
https://ijbms.mums.ac.ir/article_9621_814aed3fa1d110ca46353f4d21911fb5.pdf
2017-12-01
1331
1338
10.22038/ijbms.2017.9621
Adult bovine serum
Fetal bovine serum
PhzM
Pseudomonas aeruginosa
Pyocyanin
Aylin
Moayedi
aylinmoayedi@yahoo.com
1
Department of Microbiology, Tehran North Branch, Islamic Azad University, Tehran, Iran
AUTHOR
Jamileh
Nowroozi
nowroozij@yahoo.com
2
Department of Microbiology, Tehran North Branch, Islamic Azad University, Tehran, Iran
LEAD_AUTHOR
Abbas
Akhavan Sepahy
3
Department of Microbiology, Tehran North Branch, Islamic Azad University, Tehran, Iran
AUTHOR
1. Jander G, Rahme LG, Ausubel FM. Positive correlation between virulence of Pseudomonas aeruginosa mutants in mice and insects. J Bacteriol 2000; 182:3843-3845.
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2. Frank DW. The exoenzyme S regulon of Pseudomonas aeruginosa. Mol Microbiol 1997; 26:621-629.
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3. Budzikiewicz H. Secondary metabolites from fluorescent pseudomonads. FEMS Microbiol Rev 1993; 104:209-228.
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4. Lau GW, Hassett DJ, Ran H, Kong F. The role of pyocyanin in Pseudomonas aeruginosa infection. Trends Mol Med 2004; 10:599-606.
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5. Mavrodi DV, Bonsall RF, Delaney SM, Soule MJ, Phillips G, Thomashow LS. Functional analysis of genes for biosynthesis of pyocyanin and phenazine-1-carboxamide from Pseudomonas aeruginosa PAO1. J Bacteriol 2001; 183:6454-6465.
5
6. Whiteley M, Lee KM, Greenberg E. Identification of genes controlled by quorum sensing in Pseudomonas aeruginosa. Proc Natl Acad Sci U S A 1999; 96:13904-13909.
6
7. Gross H, Loper JE. Genomics of secondary metabolite production by pseudomonas spp. Nat Prod Rep 2009; 26:1408-1446.
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8. Muller M. Pyocyanin induces oxidative stress in human endothelial cells and modulates the glutathione redox cycle. Free Radicals Biol Med 2002; 33:1527-1533.
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9. Laursen JB, Nielsen J. Phenazine natural products: biosynthesis, synthetic analogues, and biological activity. Chem Rev 2004; 104:1663-1686.
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10. Rahme LG, Ausubel FM, Cao H, Drenkard E, Goumnerov BC, Lau GW, et al. Plants and animals share functionally common bacterial virulence factors. Proc Natl Acad Sci U S A 2000; 97:8815-8821.
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11. Anjaiah V, Koedam N, Nowak-Thompson B, Loper JE, Höfte M, Tambong JT, et al. Involvement of phenazines and anthranilate in the antagonism of Pseudomonas aeruginosa PNA1 and Tn5 derivatives toward Fusarium spp. and Pythium spp. Mol Plant-Microbe Interact 1998; 11:847-854.
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12. Kerr J, Taylor G, Rutman A, Høiby N, Cole P, Wilson R. Pseudomonas aeruginosa pyocyanin and 1-hydroxyphenazine inhibit fungal growth. J Clin Pathol 1999; 52:385-387.
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13. Rabaey K, Verstraete W. Microbial fuel cells: novel biotechnology for energy generation. Trends Biotechnol 2005; 23:291-298.
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14. Ohfuji K, Sato N, Hamada-Sato N, Kobayashi T, Imada C, Okuma H, et al. Construction of a glucose sensor based on a screen-printed electrode and a novel mediator pyocyanin from Pseudomonas aeruginosa. Biosens Bioelectron 2004; 19:1237-1244.
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15. Hassani HH, Hasan HM, Al-Saadi A, Ali AM, Muhammad MH. A comparative study on cytotoxicity and apoptotic activity of pyocyanin produced by wild type and mutant strains of Pseudomonas aeruginosa. Eur J Exp Biol 2012; 2:1389-1394.
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16. Zhao J, Wu Y, Alfred A, Wei P, Yang S. Anticancer effects of pyocyanin on HepG2 human hepatoma cells. Lett Appl Microbiol 2014; 58:541-548.
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17. Kruczek C, Qaisar U, Colmer‐Hamood JA, Hamood AN. Serum influences the expression of Pseudomonas aeruginosa quorum‐sensing genes and QS‐controlled virulence genes during early and late stages of growth. MicrobiologyOpen 2014; 3:64-79.
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18. Essar D, Eberly L, Hadero A, Crawford I. Identification and characterization of genes for a second anthranilate synthase in Pseudomonas aeruginosa: interchangeability of the two anthranilate synthases and evolutionary implications. J Bacteriol 1990; 172:884-900.
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19. Silby MW, Winstanley C, Godfrey SA, Levy SB, Jackson RW. Pseudomonas genomes: diverse and adaptable. FEMS Microbiol Rev 2011; 35:652-680.
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20. Chaerun SK, Tazaki K, Asada R, Kogure K. Bioremediation of coastal areas 5 years after the Nakhodka oil spill in the Sea of Japan: isolation and characterization of hydrocarbon-degrading bacteria. Environ Int 2004; 30:911-922.
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21. Vives-Flórez M, Garnica D. Comparison of virulence between clinical and environmental Pseudomonas aeruginosa isolates. Int Microbiol 2006; 9:247-252.
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22. El-Amine Bendaha M, Mebrek S, Naimi M, Tifrit A, Belaouni H. Isolation and comparison of rhamnolipids production in Pseudomonas aeruginosa P.B: 2 and Pseudomonas fluorescens P.V: 10. Sci Rep 2012; 1:544.
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23. Al-Hinai A, Al-Sadi A, Al-Bahry S, Mothershaw A, Al-Said F, Al-Harthi S, et al. Isolation and characterization of Pseudomonas aeruginosa with antagonistic activity against Pythium aphanidermatum. J Plant Pathol 2010; 92:653-660.
23
24. Karatuna O, Yagci A. Analysis of quorum sensing‐dependent virulence factor production and its relationship with antimicrobial susceptibility in Pseudomonas aeruginosa respiratory isolates. Clin Microbiol Infect 2010; 16:1770-1775.
24
25. Mohammed HA, Yossef HS, Mohammad FI. The cytotoxicity effect of pyocyanin on human hepatocellular carcinoma cell line (HepG2). Iraqi J Sci 2014; 55:668-674.
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26. Vinckx T, Wei Q, Matthijs S, Cornelis P. The Pseudomonas aeruginosa oxidative stress regulator OxyR influences production of pyocyanin and rhamnolipids: protective role of pyocyanin. Microbiology 2010; 156:678-686.
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27. Subramaniam L. Rapid diagnosis of Pseudomonas aeruginosa infection by demonstration of pyocyanin & fluorescein. Indian J Med Res 1985; 81:561-566.
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28. El-Fouly M, Sharaf A, Shahin A, El-Bialy HA, Omara A. Biosynthesis of pyocyanin pigment by Pseudomonas aeruginosa. J Radiat Res Appl Sci 2015; 8:36-48.
28
29. Juhas M, Wiehlmann L, Huber B, Jordan D, Lauber J, Salunkhe P, et al. Global regulation of quorum sensing and virulence by VqsR in Pseudomonas aeruginosa. Microbiology 2004; 150:831-841.
29
30. Wu L, Estrada O, Zaborina O, Bains M, Shen L, Kohler JE, et al. Recognition of host immune activation by Pseudomonas aeruginosa. Science 2005; 309:774-777.
30
ORIGINAL_ARTICLE
The role of sirolimus in proteinuria in diabetic nephropathy rats
Objective(s): The aim of this study was to observe the impact of sirolimus on proteinuria in streptozotocin (STZ) induced diabetic rats. Materials and Methods: Rats were given a single injection of STZ to induce diabetic rat model. Rats’ 24 hr urine was collected to test, urinary and the kidney tissues were harvested at the 8th and 20th weeks, respectively. Podocyte morphological changes were examined by electron microscopy and the ZO-1, podocin expressions in kidneys were detected by immunohistochemistry; the protein levels of Raptor and pS6 were measured by Western blot assay. Results: In the early stage of diabetic nephropathy (DN), sirolimus reduced the proteinuria significantly (P<0.05); but in the advanced stage of DN, sirolimus worsened proteinuria (P<0.05). Electron microscopy test suggested that sirolimus could reduce the injury of podocyte at the early DN, but increased the injury at the late DN podocyte. Immunohistochemistry results indicated that sirolimus increased the expressions of podocin and ZO-1 at the early DN (P<0.05), but reduced the expressions of ZO-1 and podocin (P<0.05) at the advanced DN. In the different periods of DN, the expression levels of Raptor and pS6 in sirolimus-treated groups were significantly lower than in the DN control groups (P<0.05). Conclusion: Sirolimus can reduce proteinuria and alleviate the early DN podocyte injury in diabetic rat model by inhibiting the activity of mTORC1; but in the advanced stage of DN, sirolimus can increase podocyte injury and urine protein level.
https://ijbms.mums.ac.ir/article_9618_c0127fa71011874e04e07e3ca33af188.pdf
2017-12-01
1339
1344
10.22038/ijbms.2017.9618
Diabetic nephropathies
mTOR protein
Podocytes
Proteinuria
Sirolimus
JinJun
Wang
meters888@163.com
1
Department of Transplantation, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, China
AUTHOR
ZiQiang
Xu
xzq6641@163.com
2
Department of Transplantation, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, China
AUTHOR
BiCheng
Chen
bisonch@163.com
3
Department of Transplantation, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, China
AUTHOR
ShaoLing
Zheng
zslhospital@163.com
4
Department of Transplantation, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, China
AUTHOR
Peng
Xia
pengxia602@163.com
5
Department of Transplantation, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, China
AUTHOR
Yong
Cai
yorkcai@126.com
6
Department of Transplantation, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, China
LEAD_AUTHOR
1. Lebranchu Y, Thierry A, Toupance O, Westeel PF, Etienne I, Thervet E, et al. Efficacy on renal function of early conversion from cyclosporine to sirolimus 3 months after renal transplantation: concept study. Am J Transplant 2009; 9:1115-1123.
1
2. Franco-Esteve A, Tordera D, de la Sen ML, Jiménez L, Mas P, Muñoz C, et al. mTOR inhibitor monotherapy. A good treatment choice in renal transplantation? Nefrologia 2012; 32:631-638.
2
3. van den Akker JM, Wetzels JF, Hoitsma AJ. Proteinuria following conversion from azathioprine to sirolimus in renal transplant recipients. Kidney Int 2006; 70:1355-1357.
3
4. Aliabadi AZ, Pohanka E, Seebacher G, Dunkler D, Kammerstätter D, Wolner E, et al. Development of proteinuria after switch to sirolimus-based immunosuppression in long-term cardiac transplant patients. Am J Transplant 2008; 8:854-861.
4
5. Letavernier E, Bruneval P, Mandet C, Duong Van Huyen JP, Péraldi MN, Helal I, et al. High sirolimus levels may induce focal segmental glomerulosclerosis de novo. Clin J Am Soc Nephrol 2007; 2:326-333.
5
6. Izzedine H, Brocheriou I, Frances C. Post-transplantation proteinuria and sirolimus. N Engl J Med 2005; 353:2088-2089.
6
7. Kaplan B, Qazi Y, Wellen JR. Strategies for the management of adverse events associated with mTOR inhibitors. Transplant Rev 2014; 28:126-133.
7
8. Kim BS, Cho Y, Lee H, Joo DJ, Huh KH, Kim MS, et al. Comparative proteomic analysis of rapamycin versus cyclosporine combination treatment in mouse podocytes. Transplant Proc 2016; 48:1297-1301.
8
9. Müller-Krebs S, Weber L, Tsobaneli J, Kihm LP, Reiser J, Zeier M, et al. Cellular effects of everolimus and sirolimus on podocytes. PLoS One 2013; 8:e80340.
9
10. Cai Y, Chen Y, Zheng S, Chen B, Yang Y, Xia P. Sirolimus damages podocytes in rats with protein overload nephropathy. J Nephrol 2011; 24:307-312.
10
11. Menini S, Iacobini C, Oddi G, Ricci C, Simonelli P, Fallucca S, et al. Increased glomerular cell (podocyte) apoptosis in rats with streptozotocin-induced diabetes mellitus: role in the development of diabetic glomerular disease. Diabetologia 2007; 50:2591-2599.
11
12. Susztak K, Raff AC, Schiffer M, Böttinger EP. Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy. Diabetes 2006; 55:225-233.
12
13. Tesch GH, Allen TJ. Rodent models of streptozotocin-induced diabetic nephropathy. Nephrology 2007; 12:261-266.
13
14. White KE, Bilous RW, Marshall SM, El Nahas M, Remuzzi G, Piras G, et al. Podocyte number in normotensive type 1 diabetic patients with albuminuria. Diabetes 2002; 51:3083-3089.
14
15. Attia DM, Feron O, Goldschmeding R, Radermakers LH, Vaziri ND, Boer P, et al. Hypercholesterolemia in rats induces podocyte stress and decreases renal cortical nitric oxide synthesis via an angiotensin II type 1 receptor-sensitive mechanism. J Am Soc Nephrol 2004; 15:949-957.
15
16. Liu XD, Zhang LY, Zhu TC, Zhang RF, Wang SL, Bao Y. Overexpression of miR-34c inhibits high glucose-induced apoptosis in podocytes by targeting Notch signaling pathways. Int J Clin Exp Pathol 2015; 8:4525-4534.
16
17. Roselli S, Gribouval O, Boute N, Sich M, Benessy F, Attié T, et al. Podocin localizes in the kidney to the slit diaphragm area. Am J Pathol 2002; 160:131-139.
17
18. Michaud JL, Lemieux LI, Dubé M, Vanderhyden BC, Robertson SJ, Kennedy CR. Focal and segmental glomerulosclerosis in mice with podocyte-specific expression of mutant alpha-actinin-4. J Am Soc Nephrol J 2003; 14:1200-1211.
18
19. Rincon-Choles H, Vasylyeva TL, Pergola PE, Bhandari B, Bhandari K, Zhang JH, et al. ZO-1 expression and phosphorylation in diabetic nephropathy. Diabetes 2006; 55:894-900.
19
20. Wullschleger S, Loewith R, Hall MN. TOR signaling in growth and metabolism. Cell 2006; 124:471-484.
20
21. Kim DH, Sabatini DM. Raptor and mTOR: subunits of a nutrient-sensitive complex. Curr Top Microbiol Immunol 2004; 279:259-270.
21
22. Thomas G. The S6 kinase signaling pathway in the control of development and growth. Biol Res 2002; 35:305-313.
22
23. Li LC, Hsu CN, Lin CC, Cheng YF, Hu TH, Chen DW, et al. Proteinuria and baseline renal function predict mortality and renal outcomes after sirolimus therapy in liver transplantation recipients. BMC Gastroenterol 2017; 17:58.
23
24. Mjörnstedt L, Sørensen SS, von Zur Mühlen B, Jespersen B, Hansen JM, Bistrup C, et al. Improved renal function after early conversion from a calcineurin inhibitor to everolimus: a randomized trial in kidney transplantation. Am J Transplant 2012; 12:2744-2753.
24
25. Mandelbrot DA, Alberú J, Barama A, Marder BA, Silva HT Jr, Flechner SM, et al. Effect of ramipril on urinary protein excretion in maintenance renal transplant patients converted to sirolimus. Am J Transplant 2015; 15:3174-3184.
25
26. Taveira-DaSilva AM, Jones AM, Julien-Williams PA, Stylianou M, Moss J. Retrospective review of combined sirolimus and simvastatin therapy in lymphangioleiomyomatosis. Chest 2015; 147:180-187.
26
27. Franco A, Más-Serrano P, Perez Contreras J, Jiménez L, Rodriguez D, Olivares J. Mammalian target of rapamycin inhibitor monotherapy: efficacy in renal transplantation. Transplant Proc 2015; 47:2364-2367.
27
28. Jun H, Kim MG, Jung CW. Clinical advantages including medication adherence with conversion to once-daily advagraf and sirolimuscombination in stable kidney recipients. Int J Clin Pharmacol Ther 2016; 54(2):81-6.
28
29. Amer H, Cosio FG. Significance and management of proteinuria in kidney transplant recipients. J Am Soc Nephrol 2009; 20:2490-2492.
29
30. Letavernier E, Bruneval P, Mandet C, Duong Van Huyen JP, Péraldi MN, Helal I, et al. High sirolimus levels may induce focal segmental glomerulosclerosis de novo. Clin J Am Soc Nephrol 2007; 2:326-333.
30
31. Godel M, Hartleben B, Herbach N, Liu S, Zschiedrich S, Lu S, et al. Role of mTOR in podocyte function and diabetic nephropathy in humans and mice. J Clin Invest 2011; 121:2197-2209.
31
32. Jefferson JA, Shankland SJ, Pichler RH. Proteinuria in diabetic kidney disease: a mechanistic viewpoint. Kidney Int 2008; 74:22-36.
32
33. Xiao T, Guan X, Nie L, Wang S, Sun L, He T, et al. Rapamycin promotes podocyte autophagy and ameliorates renal injury in diabetic mice. Mol Cell Biochem 2014; 394:145-154.
33
34. Polak P, Hall MN. mTOR and the control of whole body metabolism. Curr Opin Cell Biol 2009; 21:209-218.
34
35. Mori H, Inoki K, Masutani K, Wakabayashi Y, Komai K, Nakagawa R, et al. The mTOR pathway is highly activated in diabetic nephropathy and rapamycin has a strong therapeutic potential. Biochem Biophys Res Commun 2009; 384:471-475.
35
36. Hamatani H, Hiromura K, Sakairi T, Takahashi S, Watanabe M, Maeshima A, et al. Expression of a novel stress-inducible protein, sestrin 2, in rat glomerular parietal epithelial cells. Am J Physiol Renal Physiol 2014; 307:F708-F717.
36
ORIGINAL_ARTICLE
The effects of activated-omental extract on nuclear and cytoplasmic in vitro maturation of rat oocytes
Objective: The role of growth factors, including vascular endothelial growth factor of activated omentum on mitosis is clearly known, though not on all the aspects of in vitro oocyte maturation. This study was designed to assess the effect of activated-omental extract (AOE) on in vitro maturation (IVM) of rat cumulus-oocyte complexes (COCs). Materials and Methods: In this experimental study, the COCs were incubated in Ham’s F-10 supplemented with either 20% AOE, 20% fetal bovine serum (FBS) or serum-free media. Post-culture COCs were studied according to the cumulus cells (CCs) expansion, nuclear maturation and cytoplasmic maturation. Cumuli expansion was evaluated by inverted microscope without staining; nuclear maturation was assessed by aceto-orcein staining (light microscope) and cytoplasmic maturation was also observed by TEM. Results: Expansion of CCs and nuclear maturation of the oocytes in in vitro for 24 hr was significantly higher in AOE- and FBS-supplemented groups (P=0.000 and 0.013) and (P=0.004 and 0.014), respectively, compared to serum-free group. At ultra-structural level, after 24 hr, both FBS and AOE-supplemented media showed uniformly wide perivitelline space (PVS). After 12 hr, the cortical granules were found in the oocytes cultured in FBS and AOE-supplemented media. Within 24 hr, both granules and mitochondria were large without any detectable topographic tendency across the ooplasm. In AOE and FBS- supplemented oocytes, the number and size of microvilli were more than those in serum-free one. Conclusion: Although AOE supplementation induced a higher rate of the CCs expansion, and resuming meiosis, it was not as potent as FBS to provide cytoplasmic maturation of rat oocytes.
https://ijbms.mums.ac.ir/article_9622_3e1d88e673ae69364e54306b69fc5162.pdf
2017-12-01
1345
1353
10.22038/ijbms.2017.9622
Cumulus cells
Cytoplasm
In vitro oocyte maturation
Nucleus
Omentum
Rats
Fakhroddin
Mesbah
mesbahf@sums.ac.ir
1
Department of Anatomical Sciences, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
LEAD_AUTHOR
Aris
Donic Pracha
2
Department of Anatomical Sciences, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Tahereh
Talaei-Khozani
talaeit@sums.ac.ir
3
Department of Anatomical Sciences, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Soghra
Bahmanpour
bahmans@sums.ac.ir
4
Department of Anatomical Sciences, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
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5. Coticchio G, Dal Canto M, Fadini R, Mignini Renzini M, Guglielmo MC, Miglietta S, et al. Ultrastructure of human oocytes after in vitro maturation. Mol Hum Reprod 2016; 22:110-118.
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6. Yang YJ, Zhang YJ, Li Y. Ultrastructure of human oocytes of different maturity stages and the alteration during in vitro maturation. Fertil Steril 2009; 92:396. e1-6.
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7. Cao X, Zhou P, Luo H, Zhao Y, Shi G. The effect of VEGF on the temporal-spatial change of alpha-tubulin and cortical granules of ovine oocytes matured in vitro. Anim Reprod Sci 2009; 113:236-250.
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8. Rated M, Ketoja E, Pitkanen T, Ahola V, Kananen K, Peippo J. In vitro maturation supplements affect developmental competence of bovine cumulus-oocyte complexes and embryo quality after vitrification. Cryobiology 2011; 63:245-255.
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9. Marchal R, Caillaud M, Martoriati A, Gérard N, Mermillod P, Goudet G. Effect of growth hormone (GH) on in vitro nuclear and cytoplasmic oocyte maturation, cumulus expansion, hyaluronan synthases, and connexins 32 and 43 expression, and gh receptor messenger RNA expression in equine and porcine species. Biol Reprod 2009; 69:1013-1022.
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10.Abedelahi A, Salehnia M, Allameh AA. The effects of different concentrations of sodium selenite on the in vitro maturation of preantral follicles in serum-free and serum supplemented media. J Assist Reprod Genet 2008; 25:483-488.
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11.Sarkanan JR, Kaila V, Mannerström B, Raty S, Kuokkanen H, Miettinen S, Ylikomi T. Human adipose tissue extract induces angiogenesis and adipogenesis in vitro. Tissue Eng Part A 2012; 18:17-25.
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12.Shah S, Lowery E, Braun RK, Martin A, Huang N, Medina M, et al. Cellular basis of tissue regeneration by omentum. PLoS One 2012; 7:e38368.
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17.Zhang XW, Tao WU, Zou H, Kun W, Song-Quan H. Effect of adipose tissue extract of greater omentum on human fibroblasts in vitro. Chin J Hepat Sur 2011; 17:261-263.
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18.Araujo VR, Silva MG, Duarte AB, Magalhaes DM, Almeida AP, Goncalves RF, et al. Vascular endothelial growth factor-A165 (VEGF-A) stimulates the in vitro development and oocyte competence of goat preantral follicles. Cell Tissue Res 2011; 346:273-281.
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23.Varnosfaderani SR, Ostadhosseini S, Hajian M, Hosseini SM, Khashouei EA, Abbasi H, et al. Importance of the GDF9 signaling pathway on cumulus cell expansion and oocyte competency in sheep. Theriogenology 2013; 80:470-478.
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38
ORIGINAL_ARTICLE
The effects of specific expression of apoptin under the control of PSES and PSA promoter on cell death and apoptosis of LNCaP cells
Objective(s): Apoptotic effect of apoptin has been demonstrated in numerous studies. However, its tumor specificity has been questioned by some reports. The aim of this study was to confine the expression of apoptin in the prostate tumor cells by inducing its gene expression under the control of a chimeric enhancer composing of prostate-specific membrane antigen (PSMA) and prostate-specific antigen (PSA) regulatory elements (PSES). Furthermore, we investigated the effects of apoptin expression on LNCaP prostate carcinoma cell survival and apoptosis using MTT assay and annexinV/7-AAD flow cytometry assay. Materials and Methods: Recombinant plasmids containing apoptin gene under the control of PSES/PSA promoter or Cytomegalovirus (CMV) promoter were constructed. Tumor cell lines including LNCaP cells and HeLa cells, and LX-2 cells (as a normal control) were transfected with the plasmids and the expression of apoptin was evaluated by real time-PCR and western blot analyses. The effects of apoptin expression on cell survival and apoptosis were then investigated using MTT and annexinV/7-AAD flow cytometry assay, respectively. Results: Western blot and real time PCR analyses confirmed the specific expression of apoptin under the control of PSES/PSA regulatory element in the LNCaP cells, while CMV promoter caused apoptin expression in both tumor and normal cell lines. Apoptin expression significantly increased cell death and apoptosis in tumor cells when compared with the normal cells (P<0.001). Conclusion: These results suggest that PSES/PSA regulatory element may be considered as an efficient approach for specific expression of apoptin gene in prostate tumor cells and treatment of prostate cancer.
https://ijbms.mums.ac.ir/article_9598_df180c7c40d495721177a9a466fa59bf.pdf
2017-12-01
1354
1359
10.22038/ijbms.2017.9598
Apoptin protein
Apoptosis
Prostate-specific antigen
Prostate-specific membrane antigen
Prostate cancer
Vida
Mohammadi
vida_moh91@yahoo.com
1
Department of Medical Biotechnology, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Abbas
Behzad Behbahani
behzadbe@gmail.com
2
Department of Medical Biotechnology, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Gholam Reza
Rafiee
3
Department of Medical Biotechnology, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Seyed Younes
Hosseini
hoseiniy@sums.ac.ir
4
Department of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Marzieh
Alizadeh Zarei
5
Department of Medical Biotechnology, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Mohammad Ali
Okhovat
okhovat.clinicallab@gmail.com
6
Department of Medical Biotechnology, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Mohammad Ali
Takhshid
takhshidma@sums.ac.ir
7
Department of Medical Biotechnology, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
LEAD_AUTHOR
1. Hassanipour-Azgomi S, Mohammadian-Hafshejani A, Ghoncheh M, Towhidi F, Jamehshorani S, Salehiniya H. Incidence and mortality of prostate cancer and their relationship with the Human Development Index worldwide. Prostate Int 2016;4:118-124.
1
2. Merseburger AS, Alcaraz A, von Klot CA. Androgen deprivation therapy as backbone therapy in the management of prostate cancer. Onco Targets Ther 2016;9:7263-7274.
2
3. Heidenreich A, Bastian PJ, Bellmunt J, Bolla M, Joniau S, van der Kwast T, et al. EAU guidelines on prostate cancer. Part II: Treatment of advanced, relapsing, and castration-resistant prostate cancer. Eur Urol 2014; 65:467-479.
3
4. Marech I, Vacca A, Ranieri G, Gnoni A, Dammacco F. Novel strategies in the treatment of castration-resistant prostate cancer (Review). Int J Oncol 2012;40: 1313-1320.
4
5. Wong RS. Apoptosis in cancer: from pathogenesis to treatment. J Exp Clin Cancer Res 2011 26;30:87-101
5
6. Javan B, Shahbazi M. Hypoxia-inducible tumour-specific promoters as a dual-targeting transcriptional regulation system for cancer gene therapy. Ecancermedicalscience. 2017;11:751.
6
7. Zhong X, Zhao H, Liang S, Zhou D, Zhang W, Yuan L. Gene delivery of apoptin-derived peptide using an adeno-associated virus vector inhibits glioma and prolongs animal survival. Biochem Biophys Res Commun 2017 15;482: 506-513.
7
8. Shen Ni L, Allaudin ZN, Mohd Lila MA, Othman AM, Othman FB. Selective apoptosis induction in MCF-7 cell line by truncated minimal functional region of Apoptin. BMC cancer. 2013; 13:488.
8
9. Li X, Liu Y, Wen Z, Li C, Lu H, Tian M, et al. Potent anti-tumor effects of a dual specific oncolytic adenovirus expressing apoptin in vitro and in vivo. Mol Cancer. 2010; 9:10.
9
10. Jangamreddy JR, Panigrahi S, Lotfi K, Yadav M, Maddika S, Tripathi AK, et al. Mapping of apoptin-interaction with BCR-ABL1, and development of apoptin-based targeted therapy. Oncotarget 2014; 5 :7198-7211.
10
11. Nastasie MS, Thissen H, Jans DA, Wagstaff KM. Enhanced tumour cell nuclear targeting in a tumour progression model. BMC cancer 2015; 15:76-87.
11
12. Backendorf C, Noteborn MH. Apoptin towards safe and efficient anticancer therapies. Adv Exp Med Biol 2014;818:39-59.
12
13. Li J, Wang H, Ma Z, Fan W, Li Y, Han B, et al. TAT-Apoptin induces apoptosis in the human bladder cancer EJ cell line and regulates Bax, Bcl-2, caspase-3 and survivin expression. Exp Ther Med 2012;31033-1038.
13
14. Zhou S, Zhang M, Zhang J, Shen H, Tangsakar E, Wang J. Mechanisms of apoptin-induced cell death. Med oncol 2012;29:2985-2991.
14
15. He X, Zhang Q, Liu Y, He P. Apoptin induces chromatin condensation in normal cells. Virus genes 2005;3149-3155.
15
16. Guelen L, Paterson H, Gaken J, Meyers M, Farzaneh F, Tavassoli M. TAT-apoptin is efficiently delivered and induces apoptosis in cancer cells. Oncogene 2004; 23: 1153-1165.
16
17. Lee SJ, Kim HS, Yu R, Lee K, Gardner TA, Jung C, et al. Novel prostate-specific promoter derived from PSA and PSMA enhancers. Mole Ther 2002; 6:415-421.
17
18. Zarei MA, Takhshid M, Behbahani AB, Hosseini S, Okhovat M, Dehbidi GRR, et al. Synergistic effects of NDRG2 overexpression and radiotherapy on cell death of human prostate LNCaP cells. J Biomed Physics Eng 2016;7:257-264.
18
19. Kashkin KN, Chernov IP, Didych DA, Sverdlov ED. Construction of a combinatorial library of chimeric tumor-specific promoters. Biotechniques 2017;63:107-116.
19
20. Qi Y, Guo H, Hu N, He D, Zhang S, Chu Y, et al. Preclinical pharmacology and toxicology study of Ad-hTERT-E1a-Apoptin, a novel dual cancer-specific oncolytic adenovirus. Toxicol appl pharmacol 2014 15;280:362-369.
20
21. Leliveld SR, Dame RT, Rohn JL, Noteborn MH, Abrahams JP. Apoptin's functional N- and C-termini independently bind DNA. FEBS lett 2004 16;557:155-158.
21
22. Kucharski TJ, Gamache I, Gjoerup O, Teodoro JG. DNA damage response signaling triggers nuclear localization of the chicken anemia virus protein apoptin. J virol 2011; 85:12638-12649.
22
23. Chaabane W, Ghavami S, Malecki A, Los MJ. Human gyrovirus-Gpoptin interferes with the cell cycle and induces G2/M arrest prior to apoptosis. Arch immuno ther exp 2017:464-468.
23
ORIGINAL_ARTICLE
Vitamin E improved bone strength and bone minerals in male rats given alcohol
Objective(s): Alcohol consumption induces oxidative stress on bone, which in turn increases the risk of osteoporosis. This study determined the effects of vitamin E on bone strength and bone mineral content in alcohol-induced osteoporotic rats. Materials and Methods: Three months old Sprague Dawley male rats were randomly divided into 5 groups: (I) control group; (II) alcohol (3 g/kg) + normal saline; (III) alcohol (3 g/kg) + olive oil; (IV) alcohol (3 g/kg) + alpha-tocopherol (60 mg/kg) and (V) alcohol (3 g/kg) + palm vitamin E (60 mg/kg). The treatment lasted for three months. Following sacrifice, the right tibia was subjected to bone biomechanical test while the lumbar (fourth and fifth lumbar) and left tibia bones were harvested for bone mineral measurement. Results: Alcohol caused reduction in bone biomechanical parameters (maximum force, ultimate stress, yield stress and Young’s modulus) and bone minerals (bone calcium and magnesium) compared to control group (P<0.05). Palm vitamin E was able to improve bone biomechanical parameters by increasing the maximum force, ultimate stress and Young’s modulus (P<0.05) while alpha-tocopherol was not able to. Both alpha-tocopherol and palm vitamin E were able to significantly increase tibia calcium and magnesium content while only alpha-tocopherol caused significant increase in lumbar calcium content (P<0.05). Conclusion: Both palm vitamin E and alpha-tocopherol improved bone mineral content which was reduced by alcohol. However, only palm vitamin E was able to improve bone strength in alcohol treated rats.
https://ijbms.mums.ac.ir/article_9610_80ac61f046bcb1607e993060bf81f0c3.pdf
2017-12-01
1360
1367
10.22038/ijbms.2017.9610
Alcohol-induced disorder
Bone minerals
Bone strength
Palm oil
Vitamin E
Syuhada
Zakaria
syud.zak@gmail.com
1
Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia
AUTHOR
Siti-Zulaikha
Mat-Husain
zulaikha92_ika@yahoo.com
2
Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia
AUTHOR
Kong
Ying-Hwey
vanessa.kong@ymail.com
3
Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia
AUTHOR
Kek
Xin-Kai
kek@live.com.my
4
Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia
AUTHOR
Abdullah
Mohd-Badawi
amb_mbp@yahoo.com
5
Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia
AUTHOR
Nurul-Amiza
Abd-Ghani
pinkytm92@gmail.com
6
Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia
AUTHOR
Muhamad-Arizi
Aziz
arizi@ppukm.ukm.edu.my
7
Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia
AUTHOR
Mohamed
Norazlina
azlina@ppukm.ukm.edu.my
8
Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia
LEAD_AUTHOR
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14. Chin K, Gengatharan D, Mohd Nasru F, Khairussam R, Ern S, Aminuddin S, et al. The effects of annatto tocotrienol on bone biomechanical strength and bone calcium content in an animal model of osteoporosis due to testosterone deficiency. Nutrients 2016; 8:E808.
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17. Iwaniec UT, Turner RT, Smith BJ, Stoecker BJ, Rust A, Zhang B, et al. Evaluation of long-term vitamin E insufficiency or excess on bone mass, density, and microarchitecture in rodents. Free Radic Biol Med 2013; 65:1209–1214.
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18. Chin K-Y, Mo H, Soelaiman I-N. A review of the possible mechanisms of action of tocotrienol - a potential antiosteoporotic agent. Curr Drug Targets 2013; 14:1533–1541.
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19. Callaci J, Juknelis D, Patwardhan A, Sartori M, Frost N, Wezeman F. The effects of binge alcohol exposure on bone resorption and biomechanical and structural properties are offset by concurrent bisphosphonate treatment. Alcohol Clin Exp Res 2004; 28:182–191.
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54
ORIGINAL_ARTICLE
The effects of CCK-8S on spatial memory and long-term potentiation at CA1 during induction of stress in rats
Objective(s): Cholecystokinin (CCK) has been proposed as a mediator in stress. However, it is still not fully documented what are its effects. We aimed to evaluate the effects of systemic administration of CCK exactly before induction of stress on spatial memory and synaptic plasticity at CA1 in rats. Materials and Methods: Male Wistar rats were divided into 4 groups: the control, the control-CCK, the stress and the stress-CCK. Restraint stress was induced 6 hr per day, for 24 days. Cholecystokinin sulfated octapeptide (CCK-8S) was injected (1.6 µg/kg, IP) before each session of stress induction. Spatial memory was evaluated by Morris water maze test. Long term potentiation (LTP) in Schaffer collateral-CA1 synapses was assessed (by 100 Hz tetanization) in order to investigate synaptic plasticity. Results: Stress impaired spatial memory significantly (P<0.01). CCK in the control rats improved memory (P<0.05), and prevented the impairments in the stress group. With respect to the control group, both fEPSP amplitude and slope were significantly (P<0.05) decreased in the stress group. However, there were no differences between responses of the control–CCK and Stress–CCK groups compared to the control group. Conclusion: The present results suggest that high levels of CCK-8S during induction of stress can modulate the destructive effects of stress on hippocampal synaptic plasticity and memory. Therefore, the mediatory effects of CCK in stress are likely as compensatory responses.
https://ijbms.mums.ac.ir/article_9619_993cf8a034ea646c3fbb43cf112e9092.pdf
2017-12-01
1368
1376
10.22038/ijbms.2017.9619
CA1
Cholecystokinin sulfated octapeptide
Hippocampus
Long term potentiation
Memory
stress
Malihe
Sadeghi
sadeghimalih@gmail.com
1
Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Parham
Reisi
parhamzh@gmail.com
2
Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
LEAD_AUTHOR
Maryam
Radahmadi
m_radahmadi@med.mui.ac.ir
3
Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
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70
ORIGINAL_ARTICLE
Cytotoxic and apoptotic effects of root extract and tanshinones isolated from Perovskia abrotanoides Kar
Objective(s):Perovskia abrotanoides Kar., from family Lamiaceae, is a little known medicinal plant growing in various regions of Iran. In the present study, cryptotanshinone (CT), tanshinone 2A (Tan2A), and hydroxycryptotanshinone (HCT) were isolated and purified from the roots of P. abrotanoides. In addition, cytotoxic and apoptotic effects of total root extract (TE) and three purified tanshinones were investigated in human cervical carcinoma (HeLa) and human breast cancer (MCF-7) cell lines. Materials and Methods: Alamar Blue® assay was used to determine cell viability. Cell apoptotic rate was detected using propidium iodide staining of DNA fragmentation by flow cytometry (sub-G1 peak). The PARP cleavage, as the sign of apoptosis, was investigated by Western blotting. Results: The results revealed that CT, Tan2A, HCT, and TE exhibited significant cytotoxicity in cancer cell lines. All of these compounds caused apoptosis in treated cells and induced sub-G1 peak in the related flow cytometry histograms. HCT was found to have the highest anti-proliferative activity on cancer cells. Western blotting analysis showed cleavage of PARP protein in MCF-7 cells treated with purified tanshinones and TE after 48 hr contact with cells. Conclusion: The findings suggest that root extract of P. abrotanoides and purified tanshinones especially Tan2A and HCT have cytotoxic and apoptotic effects against cancer cell lines. So, they may serve as potential cytotoxic agents for future investigations.
https://ijbms.mums.ac.ir/article_9568_47797b0caed2de95460e3e44ab1374a5.pdf
2017-12-01
1377
1384
10.22038/ijbms.2017.9568
Apoptosis
Cytotoxicity
HeLa
MCF-7
Perovskia abrotanoides
Root extract
Tanshinone
Arehzoo
Zaker
a.zaker@alumni.um.ac.ir
1
Department of Biology, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Javad
Asili
javadasili@gmail.com
2
Department of Pharmacognosy, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Parvaneh
Abrishamchi
abrisham@um.ac.ir
3
Department of Biology, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Zahra
Tayarani-Najaran
tayraninz@mums.ac.ir
4
Medical Toxicology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Seyed Hadi
Mousavi
mousavih@mums.ac.ir;sshadim@yahoo.com
5
Medical Toxicology Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
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16.Gong Y, Li Y, Lu Y, Li L, Abdolmaleky H, Blackburn GL et al. Bioactive tanshinones in Salvia miltiorrhiza inhibit the growth of prostate cancer cells in vitro and in mice. Int J Cancer 2011; 129: 1042-1052.
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17.Park IJ, Kim MJ, Park OJ, Park MG, Choe W, Kang I et al. Cryptotanshinone sensitizes DU145 prostate cancer cells to Fas (APO1/CD95)-mediated apoptosis through Bcl-2 and MAPK regulation. Cancer Lett 2010; 298: 88-98.
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18.Jiao JW, Wen F. Tanshinone IIA acts via p38 MAPK to induce apoptosis and the down-regulation of ERCC1 and lung-resistance protein in cisplatin-resistant ovarian cancer cells. Onco Rep 2010; 25: 781-788.
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19.Lee WY, Chiu LC, Yeung JH. Cytotoxicity of major tanshinones isolated from Danshen (Salvia miltiorrhiza) on HepG2 cells in relation to glutathione perturbation. Food Chem Toxicol 2008; 46: 328–338.
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20.Tavakoli J, Miar S, Majid Zadehzare M, Akbari H. Evaluation of effectiveness of herbal Medication in cancer care: A review study. Iran J Cancer Prev 2012; 5: 144-156.
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21.Tayarani-Najaran Z, Amiri A, Karimi G, Emami SA, Asili J, Mousavi SH. Comparative studies of cytotoxic and apoptotic properties of different extracts and the essential oil of Lavandula angustifolia on malignant and normal cells. Nutr Cancer 2014; 66: 424-434.
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22.Liu JJ, Liu WD, Yang HZ, Zhang Y, Fang ZG, Liu PQ et al. Inactivation of PI3k/Akt signaling pathway and activation of caspase-3 are involved in tanshinone I-induced apoptosis in myeloid leukemia cells in vitro. Ann Hematol 2010; 89: 1089-1097.
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23.Prajitha V, Thoppil JE. Cytotoxic and apoptotic activities of extract of Amaranthus spinosus L. in Allium cepa and human erythrocytes. Cytotechnology 2017; 69:123–133.
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24.Zhou L, Chan WK, Xu N, Xiao K, Luo H, Luo KQ et al. Tanshinone IIA, an isolated compound from Salvia miltiorrhiza Bunge, induces apoptosis in HeLa cells through mitotic arrest. Life Sci 2008; 83: 394-403.
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25.Nizamutdinova IT, Lee GW, Lee JS, Cho MK, Son KH, Jeon SJ et al. Tanshinone I suppresses growth and invasion of human breast cancer cells, MDA-MB-231, through regulation of adhesion molecules. Carcinogenesis 2008; 29: 1885-1892.
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26.Kasaian J, Iranshahi M, Masullo M, Piacente S, Ebrahimi F, Iranshahi M. Sesquiterpene lactones from Ferula oopoda and their cytotoxic properties. J Asian Nat Prod Res 2014; 16: 248–253.
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28.Ashwini S, Ezhilarasan D, Anitha R. Cytotoxic effect of Caralluma fimbriata against human colon cancer cells. Pharmacogn J 2017; 9: 204-207.
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32.Mosaddik MA. In vitro cytotoxicity of tanshinones isolated from Salvia miltiorrhiza Bunge against P388 lymphocytic leukemia cells. Phytomedicine 2003; 10: 682-685.
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33.Tayarani-Najaran Z, Makki FS, Alamolhodaei NS, Mojarrab M, Emami SA. Cytotoxic and apoptotic effects of different extracts of Artemisia biennis Willd. on K562 and HL-60 cell lines. Iran J Basic Med Sci 2017; 20: 166-171.
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34.Mothana RA, Jansen R, Gruenert R, Bednarski PJ, Lindequist U. Antimicrobial and cytotoxic abietane diterpenoids from the roots of Meriandera benghalensis (Roxb.) Benth. Pharmazie 2009; 64: 613-615.
34
35.Nordin ML, Abdul Kadir A, Zakaria ZA, Othman F, Abdullah R, Abdullah MN. Cytotoxicity and apoptosis induction of Ardisia crispa and its solvent partitions against Mus musculus mammary carcinoma cell line (4T1). Evid Based Complement Alternat Med 2017; 2017:9368079.
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37.Tayarani-Najaran Z, Emami SA, Asili J, Mirzaei A, Mousavi SH. Analyzing cytotoxic and apoptogenic properties of Scutellaria litwinowii root extract on cancer cell lines. Evid Based Complement Alternat Med 2011; 2011:160682.
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38.Yoon Y, Kim YO, Jeon WK, Park HJ, Sung HJ. Tanshinone IIA isolated from Salvia miltiorrhiza Bunge induced apoptosis in HL60 human premyelocytic leukemia cell line. J Ethnopharmacol 1999; 68: 121-127.
38
ORIGINAL_ARTICLE
Sodium hydrosulfide upregulates mRNA and protein expression of TGF-α in gastric mucosa in experimental model of stimulated gastric acid secretion in rats
Objective(s): Transforming growth factor alpha (TGF-α) has been shown to modulate the gastric acid secretion. Therefore, the aim of the present study was to investigate the effect of sodium hydrosulfide (NaHS) on TGF-α expression in gastric mucosa in rats. Materials and Methods: Eighteen rats were randomly divided into 3 groups (6 per group). To determine the effect of NaHS on gene and protein expression of TGF-α in gastric mucosa in response to gastric acid, the acid output induced by gastric distension. At the end of experiment, rats were euthanized by anesthetics, and gastric effluents, in addition to mucosa were collected to measure the pH of gastric effluents and to quantify protein and gene expression of TGF-α. Results: The stimulated gastric acid upregulated expression levels of TGF-α in gastric mucosa. These levels were higher in animals pretreated with NaHS. Conclusion: TGF-α upregulatory effect of sodium hydrosulfate implied that TGF-α is involved in the acid inhibitory effect of NaHS.
https://ijbms.mums.ac.ir/article_9597_8718bb7eb9ba2b0a21f945814a931c7f.pdf
2017-12-01
1385
1389
10.22038/ijbms.2017.9597
Gastric acid secretion
NaHS
Rat
TGF-α
Western blot
Ghaidafeh
Akbari
akbari.gh@ajums.ac.ir
1
Physiology Research Center (PRC), Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
AUTHOR
Seyyed Ali
Mard
alimard77@gmail.com;mard-sa@ajums.ac.ir
2
Research Center for Infectious Diseases of Digestive System [Alimentary Tract Research Center], Physiology Research Center (PRC), Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
LEAD_AUTHOR
Seyed Esmaeil
Khoshnam
3
Physiology Research Center (PRC), Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
AUTHOR
Iraj
Ahmadi
ahmadiiraj57@yahoo.com
4
Physiology Research Center (PRC), Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
AUTHOR
1. Celikel C, Eren F, Gulluoglu B, Bekiroglu N, Turhal S. Relation of neuroendocrine cells to transforming growth factor-alpha and epidermal growth factor receptor expression in gastric adenocarcinomas: prognostic implications. Pathol Oncol Res 2007;13:215-226.
1
2. Goldenring JR, Tsunoda Y, Stoch SA, Coffey RJ, Modlin IM. Transforming growth factor-alpha (TGFα) inhibition of parietal cell secretion: structural requirements for activity. Regul Pept 1993;43:37-47.
2
3. Kelly E, Newell S, Brownlee K, Farmery S, Cullinane C, Reid W, et al. Role of epidermal growth factor and transforming growth factor α in the developing stomach. Arch Dis Child Fetal Neonatal Ed 1997;76: 158-162.
3
4. Coffey RJ, Romano M, Polk W, Dempsey P. Roles for transforming growth factor-alpha in gastric physiology and pathophysiology. Yale J Biol Med 1992; 65: 693–623.
4
5. Beauchamp R, Barnard J, McCutchen C, Cherner J, Coffey Jr R. Localization of transforming growth factor alpha and its receptor in gastric mucosal cells. Implications for a regulatory role in acid secretion and mucosal renewal. J Clin Invest. 1989 84; 3: 1017–1023.
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6. Hoffmann P, Zeeh J, Lakshmanan J, Wu V, Procaccino F, Reinshagen M, et al. Increased expression of transforming growth factor α precursors in acute experimental colitis in rats. Gut 1997; 41:195-202.
6
7. Miettinen PJ. Transforming growth factor-α and epidermal growth factor expression in human fetal gastrointestinal tract. Pediatr Res 1993 33; 5: 481-486.
7
8. Romano M, Lesch CA, Meise KS, Veljaca M, Sanchez B, Kraus ER, et al. Increased gastroduodenal concentrations of transforming growth factor alpha in adaptation to aspirin in monkeys and rats. Gastroenterology. 1996;110:1448-1455.
8
9. John DS, Yeomans N, McDermott F, De Boer W. Adaptation of the gastric mucosa to repeated administration of aspirin in the rat. Am J Dig Dis 1973;18: 881-885.
9
10. Takeuchi K, Ise F, Takahashi K, Aihara E, Hayashi S. H2S-induced HCO3− secretion in the rat stomach–Involvement of nitric oxide, prostaglandins, and capsaicin-sensitive sensory neurons. Nitric Oxide 2015;46:157-164.
10
11. Mard SA, Veisi A, Ahangarpour A, Gharib-Naseri MK. Gastric acid induces mucosal H2S release in rats by upregulating mRNA and protein expression of cystathionine gamma lyase. J Physiol Sci 2015;65:545-554.
11
12. Mard SA, Askari H, Neisi N, Veisi A. Antisecretory effect of hydrogen sulfide on gastric acid secretion and the involvement of nitric oxide. Biomed Res Int 2014;2014:480921.
12
13. Mard SA, Godarzinejad H, Dianat M. Duodenal acidification stimulates gastric H2S release through upregulating mRNA expression of cystathionine gamma lyase. Physiology and Pharmacology 2016;20:57-62.
13
14. Enokido Y, Suzuki E, Iwasawa K, Namekata K, Okazawa H, Kimura H. Cystathionine β-synthase, a key enzyme for homocysteine metabolism, is preferentially expressed in the radial glia/astrocyte lineage of developing mouse CNS. The FASEB J 2005;19:1854-1856.
14
15. Kimura H, Shibuya N, Kimura Y. Hydrogen sulfide is a signaling molecule and a cytoprotectant. Antioxid Redox Signal 2012;17:45-57.
15
16. Mard SA, Veisi A, Ahangarpour A, Gharib-Naseri MK. Mucosal acidification increases hydrogen sulfide release through up-regulating gene and protein expressions of cystathionine gamma-lyase in the rat gastric mucosa. Iran J Basic Med Sci 2016;19:172-177.
16
17. Akbari G, Mard SA, Dianat M, Mansouri E. The Hepatoprotective and MicroRNAs Downregulatory Effects of Crocin Following Hepatic Ischemia-Reperfusion Injury in Rats. Oxid Med Cell Longev 2017;2017:1702967.
17
18. Niazmand S, Khooshnood E, Derakhshan M. Effects of Achillea wilhelmsii on rat’s gastric acid output at basal, vagotomized, and vagal-stimulated conditions. Pharmacogn Mag 2010;6:282-285.
18
19. Guo S, Gao Q, Jiao Q, Hao W, Gao X, Cao J-M. Gastric mucosal damage in water immersion stress: mechanism and prevention with GHRP-6. World J Gastroenterol 2012;18:3145-3155.
19
20. Konturek P, Ernst H, Brzozowski T, Ihlm A, Hahn E, Konturek S. Expression of epidermal growth factor and transforming growth factor-α after exposure of rat gastric mucosa to stress. Scand J Gastroenterol 1996;31:209-216.
20
21. Rhodes JA, Tam JP, Finke U, Saunders M, Bernanke J, Silen W, et al. Transforming growth factor alpha inhibits secretion of gastric acid. Proc Natl Acad Sci U S A. 1986; 83: 3844–3846.
21
22. Mard SA, Neisi N, Solgi G, Hassanpour M, Darbor M, Maleki M. Gastroprotective effect of NaHS against mucosal lesions induced by ischemia–reperfusion injury in rat. Dig Dis Sci 2012 ;57:1496-1503
22
23. Yonezawa D, Sekiguchi F, Miyamoto M, Taniguchi E, Honjo M, Masuko T, et al. A protective role of hydrogen sulfide against oxidative stress in rat gastric mucosal epithelium. Toxicology 2007;241:11-18.
23
24. Bastaki S, Chandranath S, Singh J. Comparison of the antisecretory and antiulcer activity of epidermal growth factor, urogastrone andt ransforming growth factor alpha and its derivative in rodents in vivo. Mol Cell Biochem 2002;236:83-94.
24
25. Grupcev G, Wallin C, Emås S, Theodorsson E, Hellström P. Transforming growth factor-α and epidermal growth factor inhibit gastric acid secretion and stimulate release of somatostatin and neurotensin in the conscious rat. Regul Pept 1994;14;52:111-118.
25
26. Berg A, Redeen S, Ericson A-C, Sjöstrand SE. Nitric oxide-an endogenous inhibitor of gastric acid secretion in isolated human gastric glands. BMC Gastroenterol 2004;4:16.
26
27. Arebi N, Healey ZV, Bliss PW, Ghatei M, Van Noorden S, Playford RJ, et al. Nitric oxide regulates the release of somatostatin from cultured gastric rabbit primary D-cells. Gastroenterology 2002;123:566-576.
27
ORIGINAL_ARTICLE
Anti-hyperglycemic and antioxidant potential of Croton bonplandianus. Bail fractions in correlation with polyphenol content
Objective(s):Diabetes mellitus, a carbohydrate metabolic disorder, occurs due to absolute or relative deficiency of insulin. Current treatment strategies involve either preventing or delaying the intestinal absorption of glucose to lower the levels of postprandial hyperglycemia (PPHG). Herbal remedies have been since ancient times for treating diabetes mellitus. Therefore, identifying novel phytocompounds with α-amylase and α-glucosidase inhibitory activity that would reduce the glucose absorption as well as the rise in postprandial blood glucose level is vital. Consequently, the present study was aimed to investigate the anti-hyperglycemic activity of Croton bonplandianusagainst these pancreatic enzymes. Materials and Methods: The methanol extract of C. bonplandianusleaf was prepared and further fractionation was performed with n-hexane, ethyl acetate and chloroform. The antioxidant activity and anti-hyperglycemic activity of the extracts and its fractions were determined. Further, GC-MS analysis was performed for the leaf extract. Results:The chloroform fraction (ChF) was found to contain highest quantity of polyphenols (114.28 µg/ml of GAE), flavonoids (95.68 µg/ml of quercetin) and tannins (63.80 µg/ml of GAE) and also possessed effective inhibitory activity against α amylase (IC5095.78 µg/ml) and α glucosidase (IC50 126.81 µg/ml). The antioxidant activity of ChFwas also higher when compared to other fractions. Further, GC-MS analysis of ChF showed the presence of various components that may be responsible for the above mentioned activities. Conclusion:The study findings suggest that the components present in the leaves of C. bonplandianus, may provide a potential therapeutic source in developing treatment forhyperglycemia. Further bioassay guided fractionation procedure is required to identify the active constituents.
https://ijbms.mums.ac.ir/article_9623_660c6cccced91b7e7fe679c2f95d544d.pdf
2017-12-01
1390
1397
10.22038/ijbms.2017.9623
Antihyperglycemia
α-Amylase
α-Glucosidase
Polyphenols
Postprandial hyperglycemia
Uma Dharshini
Karuppiah Vijayamuthuramalingam
1
Department of Biomedical Sciences, Sri Ramachandra University, Porur, Chennai, India
AUTHOR
Rajeswari
Rajaram
2
Department of Biomedical Sciences, Sri Ramachandra University, Porur, Chennai, India
AUTHOR
Kalaivani Madhavaram
Kuppusamy
3
Department of Biomedical Sciences, Sri Ramachandra University, Porur, Chennai, India
AUTHOR
Bhavana
Jonnalagadda
4
Department of Biomedical Sciences, Sri Ramachandra University, Porur, Chennai, India
AUTHOR
Sumathy
Arokiasamy
sumathyjoseph04@sriramachandra.edu.in
5
Department of Biomedical Sciences, Sri Ramachandra University, Porur, Chennai, India
LEAD_AUTHOR
1. Chauhan A, Sharma PK, Srivastava P, Kumar N, Dudhe R. Plants having potential antidiabetic activity: a review. Der Pharm Lett 2010; 2:369-387.
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5. Sangeetha R, Vedasree N. In vitro α-amylase inhibitory activity of the leaves of Thespesiapopulnea. ISRN Pharmacol 2012; 2012:515634.
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7. Mohamed EA, Siddiqui MJ, Ang LF, Sadikun A, Chan SH, Tan SC, et al. Potent α-glucosidase and α-amylase inhibitory activities of standardized 50% ethanolic extracts and sinensetin from OrthosiphonstamineusBenth as anti-diabetic mechanism. BMC Complement Altern Med 2012; 12:176-182.
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11. Keerthana G, Kalaivani MK, Sumathy A. In vitro alpha amylase inhibitory and anti- oxidant activities of ethanolic leaf extract of Croton bonplandianus. Asian J Pharm Clin Res 2013; 6:32-36.
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13. Tiwari P, Kumar B, Kaur M, Kaur G, Kaur H. Phytochemical screening and extraction: a review. Int Pharm Sci 2011; 1:98-106.
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14. Jain A, Sharma P, Sunil K. Evaluation of phenolic and flavonoid profile and screening of antioxidant activity of the plant Croton sparsiflorus by bio-autographic method. J Pharm Res 2010; 3:1146-1148.
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19. Kazeem MI, Adamson JO, Ogunwande IA. Modes of inhibition of α-Amylase and α-glucosidase by aqueous extract of MorindalucidaBenth leaf. BioMed Res Int 2013; 2013:1–6.
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20. Bachhawat JA, Shihabudeen MS, Thirumurugan K. Screening of fifteen Indian ayurvedic plants for α-glucosidase inhibitory activity and enzyme kinetics. Int J Pharm PharmSci 2011; 3:267-274.
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21. Cheng AY, Fantus IG. Oral antihyperglycemic therapy for type 2 diabetes mellitus. CMAJ 2005; 172:213-226.
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22. De Sousa E, Zanatta L, Seifriz I, Creczynski-Pasa TB, Pizzolatti MG, Szpoganicz B, et al. Hypoglycemic effect and antioxidant potential of Kaempferol-3,7-O-(α)-dirhamnoside from Bauhinia forficataLeaves. J Nat Prod 2004; 67:829–832.
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23. Mai TT, Fumie N, Chuyen NV. Antioxidant activities and hypolipidemic effects of an aqueous extract from flower buds of Cleistocalyxoperculatus (Roxb.) merr. andperry. J Food Biochem 2009; 33:790-807.
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24. Perera HK, Premadasa WK, Poongunran J. α-glucosidase and glycation inhibitory effects of Costusspeciosus leaves. BMC Complement Altern Med 2016; 16:2.
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26. Fukuda T, Ito H, Yoshida T. Effect of the walnut polyphenol fraction on oxidative stress in type 2 diabetes mice. Biofactors 2004; 21:251-253.
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27. Pérez-Matute P, Zulet MA, Martínez JA. Reactive species and diabetes: counteracting oxidative stress to improve health. CurrOpinPharmacol 2009; 9:771-779.
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28. Gundimeda U, McNeill TH, Elhiani AA, Schiffman JE, Hinton DR, Gopalakrishna R. Green tea polyphenols precondition against cell death induced by oxygen-glucose deprivation via stimulation of laminin receptor, generation of reactive oxygen species, and activation of protein kinase cϵ. J BiolChem 2012; 287:34694-34708.
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29. Sales PM, Souza PM, Simeoni LA, Silveira D. α-Amylase inhibitors: a review of raw material and isolated compounds from plant source. J Pharm PharmSci 2012; 15:141-183.
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33. Tundis R, Menichini F, Loizzo MR, Bonesi M, Solimene U, Menichini F. Studies on the potential antioxidant properties of SeneciostabianusLacaita (Asteraceae) and its inhibitory activity against carbohydrate-hydrolysing enzymes. Nat Product Res 2012; 26:393-404.
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34
ORIGINAL_ARTICLE
Contributors (Peer Reviewers)
https://ijbms.mums.ac.ir/article_9624_4796e1a2049d042929d649a10a9d91c6.pdf
2017-12-01
1398
1400
10.22038/ijbms.2017.9624