ORIGINAL_ARTICLE
Medicinal herbs in the treatment of neuropathic pain: a review
Chronic neuropathic pain is a common significant and debilitating problem that presents a major challenge to health-care. Despite the large number of available drugs, there are no curative conventional treatments for neuropathic pain. Nowadays, more attention has been focused on the herbal formulation in the field of drug discovery. Therefore, we performed an extensive review about herbal drugs and plants that exhibited protective effects on neuropathic pain. In this review, the beneficial effects of each plant in different neuropathic pain model, either in animals or in patients are reported. Moreover, the possible involved mechanisms for the protective effects are discussed. The more common plants which are used for the treatment of neuropathic pain are included as: Acorus calamus, Artemisia dracunculus, Butea monosperma, Citrullus colocynthis, Curcuma longa, Crocus sativus, Elaeagnus angustifolia, Ginkgo biloba, Mitragyna speciosa, Momordica charantia, Nigella sativa, Ocimum sanctum, Phyllanthus amarus, Pterodon pubescens Benth, Rubia cordifolia and Salvia officinalis. Furthermore, the most pathways which are known to be involved in pain relief by means of herbal remedies are anti-oxidant activity, anti-inflammatory, anti-apoptotic, neuroprotective and calcium inhibitory actions.In conclusion, this review suggests that some herbal plants can be suitable candidates for the treatment of neuropathic pain.
https://ijbms.mums.ac.ir/article_10461_eb6fe7069bbd11308a2779137b661bb0.pdf
2018-04-01
347
358
10.22038/ijbms.2018.24026.6021
Analgesic
Antinociceptive
Chronic pain
Herbal medicine Neuropathic pain
Fatemeh
Forouzanfar
forouzanfarf901@mums.ac.ir
1
Department of Neuroscience, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
hossein
hosseinzadeh
hosseinzadehh@mums.ac.ir
2
Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
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118. Qiu H-Q, Xu Y, Jin G-L, Yang J, Liu M, Li S-P, et al. Koumine enhances spinal cord 3α-hydroxysteroid oxidoreductase expression and activity in a rat model of neuropathic pain. Mol Pain 2015;11:1-13.
118
119. Ling Q, Liu M, Wu M-X, Xu Y, Yang J, Huang H-H, et al. Anti-allodynic and neuroprotective effects of koumine, a Benth alkaloid, in a rat model of diabetic neuropathy. Biol Pharm Bull 2014;37:858-864.
119
120. Kandhare AD, Raygude KS, Ghosh P, Ghule AE, Bodhankar SL. Neuroprotective effect of naringin by modulation of endogenous biomarkers in streptozotocin induced painful diabetic neuropathy. Fitoterapia 2012;83:650-659.
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121. Hu CY, Zhao YT. Analgesic effects of naringenin in rats with spinal nerve ligation‑induced neuropathic pain. Biomed Rep 2014;2:569-573.
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122. Liu X, Liu M, Mo Y, Peng H, Gong J, Li Z, et al. Naringin ameliorates cognitive deficits in streptozotocin-induced diabetic rats. Iran J Basic Med Sci 2016;19:411-416.
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123. Anjaneyulu M, Chopra K. Quercetin, a bioflavonoid, attenuates thermal hyperalgesia in a mouse model of diabetic neuropathic pain. Prog Neuropsychopharmacol Biol Psychiatry 2003;27:1001-1005.
123
124. Qu L, Liang X, Gu B, Liu W. Quercetin alleviates high glucose-induced Schwann cell damage by autophagy. Neural Regener Res 2014;9:1195-203.
124
125. Elbe H, Vardi N, Esrefoglu M, Ates B, Yologlu S, Taskapan C. Amelioration of streptozotocin-induced diabetic nephropathy by melatonin, quercetin, and resveratrol in rats. Hum Exp Toxicol 2015;34:100-113.
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126. Civi S, Emmez G, Dere UA, Borcek AO, Emmez H. Effects of quercetin on chronic constriction nerve injury in an experimental rat model. Acta Neurochir 2016;158:959-965.
126
ORIGINAL_ARTICLE
Trans-chalcone enhances insulin sensitivity through the miR-34a/SIRT1 pathway
Objective(s): Trans-chalcone as the parent member of the chalcone series reduces circulating levels of insulin and glucose. However, the cellular mechanism of these effects is poorly understood. Sirtuin 1 (SIRT1) as a direct target of miR-34a controls homeostasis of glucose, and also improves insulin sensitivity. Therefore, the present study for the first time investigated the influence of trans-chalcone on the miR-34a/SIRT1 pathway as a possible mechanism for its hypoglycemic and hypoinsulinemic effects. Materials and Methods: In this study, thirty male rats were randomly divided into three groups (n=10): solvent control (NS), oral administration of trans-chalcone for 2 (N2T) and 6 weeks (N6T) groups. Then, hepatic levels of miR-34a and SIRT1 were measured through the qRT-PCR method.Results: Trans-chalcone reduced food intake, body weight gain, and serum glucose as well as insulin levels. Also, this chalcone inhibited hepatic miR-34a expression and significantly elevated SIRT1 mRNA level. Conclusion: Trans-chalcone as an insulin-sensitizing chalcone partly acts through the miR-34a/SIRT1 pathway.
https://ijbms.mums.ac.ir/article_10332_61c5d41bd0c99e547af5ff711d7c5e26.pdf
2018-04-01
359
363
10.22038/ijbms.2018.24300.6063
Liver
MiR-34a
Rat
SIRT1
Trans-chalcone
Elham
Karimi Sales
karimi.sales@gmail.com
1
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Sajad
Jeddi
sajad.jeddy62@gmail.com
2
Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Abbas
Ebrahimi-Kalan
ebrahimiab@tbzmed.ac.ir
3
Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Mohammad Reza
Alipour
alipourmr52@gmail.com
4
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
LEAD_AUTHOR
1. Matos MJ, Vazquez-Rodriguez S, Uriarte E, Santana L. Potential pharmacological uses of chalcones: a patent review (from June 2011 – 2014). Expert Opin Ther Pat 2015; 25:351-366.
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2. Orlikova B, Tasdemir D, Golais F, Dicato M, Diederich M. Dietary chalcones with chemopreventive and chemotherapeutic potential. Genes Nutr 2011; 6:125-147.
2
3. Singh H, Sidhu S, Chopra K, Khan M. Hepatoprotective effect of trans-chalcone on experimentally induced hepatic injury in rats: inhibition of hepatic inflammation and fibrosis. Can J Physiol Pharma 2016; 94:879-887.
3
4. Jalalvand F, Amoli MM, Yaghmaei P, Kimiagar M, Ebrahim-Habibi A. Acarbose versus trans-chalcone: comparing the effect of two glycosidase inhibitors on obese mice. Arch Endocrinol Metab 2015; 59:202-209.
4
5. Batovska DI, Todorova IT. Trends in utilization of the pharmacological potential of chalcones. Curr Clin Pharmacol 2010; 5:1-29.
5
6. Aksöz BE, Ertan R. Chemical and Structural Properties of Chalcones I. FABAD J Pharm Sci 2011; 36:223-242.
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7. Rahman MA. Chalcone: A valuable insight into the recent advances and potential pharmacological activities. Chem Sci J 2011; 2011:CSJ-29.
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8. Yaghmaei P, Kheirbakhsh R, Dezfulian M, Haeri-Rohani A, Larijani B, Ebrahim-Habibi A. Indole and trans-chalcone attenuate amyloid β plaque accumulation in male Wistar rat: in vivo effectiveness of two anti-amyloid scaffolds. Arch Ital Biol 2013; 151:106-113.
8
9. Najafian M, Ebrahim-Habibi A, Yaghmaei P, Parivar K, Larijani B. Core structure of flavonoids precursor as an antihyperglycemic and antihyperlipidemic agent: an in vivo study in rats. Acta Biochim Pol 2010; 57:553-560.
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10. Liang F, Kume S, Koya D. SIRT1 and insulin resistance. Nat Rev Endocrinol 2009; 5:367-373.
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11. Chen YR, Fang SR, Fu YC, Zhou XH, Xu MY, Xu WC. Calorie restriction on insulin resistance and expression of SIRT1 and SIRT4 in rats. Biochem Cell Biol 2010; 88:715-722.
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12. Chakraborty C, Doss CG, Bandyopadhyay S, Agoramoorthy G. Influence of miRNA in insulin signaling pathway and insulin resistance: micro-molecules with a major role in type-2 diabetes. Wiley Interdiscip Rev RNA 2014; 5:697-712.
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13. Choi SE, Fu T, Seok S, Kim DH, Yu E, Lee KW, et al. Elevated microRNA-34a in obesity reduces NAD+ levels and SIRT1 activity by directly targeting NAMPT. Aging Cell 2013; 12:1062-1072.
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14. Sun C, Zhang F, Ge X, Yan T, Chen X, Shi X, et al. SIRT1 improves insulin sensitivity under insulin-resistant conditions by repressing PTP1B. Cell Metab 2007; 6:307-319.
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15. Guarente L. Sirtuins, aging, and metabolism. Cold Spring Harb Symp Quant Biol 2011; 76:81-90.
15
16. Castro RE, Ferreira DM, Afonso MB, Borralho PM, Machado MV, Cortez-Pinto H, et al. MiR-34a/SIRT1/p53 is suppressed by ursodeoxycholic acid in the rat liver and activated by disease severity in human non-alcoholic fatty liver disease. J Hepatol 2013; 58:119-125.
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17. Guarente L. Sirtuins as potential targets for metabolic syndrome. Nature 2006; 444:868-874.
17
18. Klover PJ, Mooney RA. Hepatocytes: critical for glucose homeostasis. Int J Biochem Cell B 2004; 36:753-758.
18
19. Yang YM, Seo SY, Kim TH, Kim SG. Decrease of microRNA-122 causes hepatic insulin resistance by inducing protein tyrosine phosphatase 1B, which is reversed by licorice flavonoid. Hepatology 2012; 56:2209-2220.
19
20. Baselga-Escudero L, Arola-Arnal A, Pascual-Serrano A, Ribas-Latre A, Casanova E, Salvado MJ, et al. Chronic administration of proanthocyanidins or docosahexaenoic acid reverses the increase of miR-33a and miR-122 in dyslipidemic obese rats. PLoS One 2013; 8:e69817.
20
21. Baselga‐Escudero L, Bladé C, Ribas‐Latre A, Casanova E, Salvadó MJ, Arola L, et al. Grape seed proanthocyanidins repress the hepatic lipid regulators miR‐33 and miR‐122 in rats. Mol Nutr Food Res 2012; 56:1636-1646.
21
22. Baselga-Escudero L, Pascual-Serrano A, Ribas-Latre A, Casanova E, Salvadó MJ, Arola L, et al. Long-term supplementation with a low dose of proanthocyanidins normalized liver miR-33a and miR-122 levels in high-fat diet–induced obese rats. Nutr Res 2015; 35:337-345.
22
23. Baselga-Escudero L, Blade C, Ribas-Latre A, Casanova E, Suarez M, Torres JL, et al. Resveratrol and EGCG bind directly and distinctively to miR-33a and miR-122 and modulate divergently their levels in hepatic cells. Nucleic Acids Res 2014; 42:882-892.
23
24. Joven J, Espinel E, Rull A, Aragonès G, Rodríguez-Gallego E, Camps J, et al. Plant-derived polyphenols regulate expression of miRNA paralogs miR-103/107 and miR-122 and prevent diet-induced fatty liver disease in hyperlipidemic mice. BBA-Gen Subjects 2012; 1820:894-899.
24
25. Baselga-Escudero L, Blade C, Ribas-Latre A, Casanova E, Salvadó M-J, Arola L, et al. Chronic supplementation of proanthocyanidins reduces postprandial lipemia and liver miR-33a and miR-122 levels in a dose-dependent manner in healthy rats. J Nutr Biochem 2014; 25:151-156.
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26. Okunrobo LO, Usifoh CO, Uwaya JO. Anti-inflammatory and gastroprotective properties of some chalcones. Acta Pol Pharm 2006; 63:195-199.
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27. Yousefzadeh N, Jeddi S, Alipour MR. Effect of Fetal Hypothyroidism on Cardiac Myosin Heavy Chain Expression in Male Rats. Arq Bras Cardiol 2016; 107:147-153.
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28. Habibi P, Alihemmati AR, Nasirzadeh MR, Yousefi H, Habibi MR, Ahmadiasl N. Involvement of microRNA-133 and -29 in cardiac disturbances in diabetic ovariectomized rats. Iran J Basic Med Sci 2016; 19:1177-1185.
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29. Wedick NM, Pan A, Cassidy A, Rimm EB, Sampson L, Rosner B, et al. Dietary flavonoid intakes and risk of type 2 diabetes in US men and women. Am J Clin Nutr 2012; 95:925-933.
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30. Knekt P, Kumpulainen J, Jarvinen R, Rissanen H, Heliovaara M, Reunanen A, et al. Flavonoid intake and risk of chronic diseases. Am J Clin Nutr 2002; 76:560-568.
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31. Karkhaneh L, Yaghmaei P, Parivar K, Sadeghizadeh M, Ebrahim-Habibi A. Effect of trans-chalcone on atheroma plaque formation, liver fibrosis and adiponectin gene expression in cholesterol-fed NMRI mice. Pharmacol Rep 2016; 68:720-727.
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32. Shrime MG, Bauer SR, McDonald AC, Chowdhury NH, Coltart CE, Ding EL. Flavonoid-rich cocoa consumption affects multiple cardiovascular risk factors in a meta-analysis of short-term studies. J Nutr 2011; 141:1982-1988.
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33. Curtis PJ, Sampson M, Potter J, Dhatariya K, Kroon PA, Cassidy A. Chronic ingestion of flavan-3-ols and isoflavones improves insulin sensitivity and lipoprotein status and attenuates estimated 10-year CVD risk in medicated postmenopausal women with type 2 diabetes: a 1-year, double-blind, randomized, controlled trial. Diabetes Care 2012; 35:226-232.
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34. Ding J, Li M, Wan X, Jin X, Chen S, Yu C, et al. Effect of miR-34a in regulating steatosis by targeting PPARα expression in nonalcoholic fatty liver disease. Sci Rep 2015; 5:13729.
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35. Rokavec M, Li H, Jiang L, Hermeking H. The p53/miR-34 axis in development and disease. J Mol Cell Biol 2014; 6:214-230.
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36. Price NL, Ramírez CM, Fernández-Hernando C. Relevance of microRNA in metabolic diseases. Crit Rev Cl Lab Sci 2014; 51:305-320.
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37. Davis JM, Murphy EA, Carmichael MD, Davis B. Quercetin increases brain and muscle mitochondrial biogenesis and exercise tolerance. Am J Physiol Regul Integr Comp Physiol 2009; 296:R1071-1077.
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38. Zhang ZF, Zhang YQ, Fan SH, Zhuang J, Zheng YL, Lu J, et al. Troxerutin protects against 2,2’,4,4’-tetrabromodiphenyl ether (BDE-47)-induced liver inflammation by attenuating oxidative stress-mediated NAD(+)-depletion. J Hazard Mater 2015; 283:98-109.
38
39. Kahyo T, Ichikawa S, Hatanaka T, Yamada MK, Setou M. A novel chalcone polyphenol inhibits the deacetylase activity of SIRT1 and cell growth in HEK293T cells. J Pharmacol Sci 2008; 108:364-371.
39
ORIGINAL_ARTICLE
5-BDBD ameliorates an OVA-induced allergic asthma by the reduction of Th2 cytokines production
Objective(s): P2X4R is expressed in immunocyte and lung tissues. It has been a focus in inflammatory responses recently. This study investigated whether blockage of P2X4R attenuates allergic inflammation by modulating T cell response in ovalbumin-sensitized mice. Materials and Methods: Ovalbumin was used to sensitize and challenge for a mouse model. Intranasal application of 5-BDBD, P2X4R antagonist, were performed 3 hr before each airway allergen challenge. The lung was evaluated for P2X4R by real-time PCR and immunofluorescence. Th1/Th2 cytokines in bronchoalveolar lavage fluid were measured by ELISA. T-bet, Gata-3, and p-p38 MAPK were measured by Western blot or real-time PCR. Results: P2X4R was overexpressed in the lung after allergen challenge compared with the control group. Blockage of P2X4R decreased inflammation in the lung, IL-4 expression was reduced as well as IL-5; IFN-γ expression was elevated in BALF in ovalbumin-sensitized mice. Moreover, blockage of P2X4R inhibited ovalbumin-induced increased Gata-3 level and decreased T-bet level. Conclusion: These findings suggest that 5-BDBD ameliorates an ovalbumin-induced asthmatic attack by the downregulation of cytokines related to the Th2 cell.
https://ijbms.mums.ac.ir/article_10373_238968e1f33d40510d4441cf2cb53126.pdf
2018-04-01
364
369
10.22038/ijbms.2018.25731.6345
5-BDBD
Asthma
Gata-3
T-bet
Th2 cells
Bing
Hu
15776596195@163.com
1
Department of Anatomy, Harbin Medical University Daqing, Daqing, 163319, Heilongjiang Province, China
AUTHOR
Xiaoqian
Feng
fengxiaoqian@163.com
2
Department of Pathology, Harbin Medical University Daqing, Daqing 163319, Heilongjiang Province, China
AUTHOR
Li
Wang
wangli4462@163.com
3
Department of Anatomy, Harbin Medical University Daqing, Daqing, 163319, Heilongjiang Province, China
AUTHOR
Yinli
Song
syl3127@126.com
4
Department of Pathology, Harbin Medical University Daqing, Daqing 163319, Heilongjiang Province, China
AUTHOR
Xiuqin
Ni
nxq200285@163.com
5
Department of Anatomy, Harbin Medical University Daqing, Daqing, 163319, Heilongjiang Province, China
LEAD_AUTHOR
1. Elias JA, Zhu Z, Chupp G, Homer RJ. Airway remodeling in asthma. J Clin Invest 1999; 104:1001-1006.
1
2. Jeffery PK. Remodeling in asthma and chronic obstructive lung disease. Am J Respir Crit Care Med 2001; 164:S28-38.
2
3. Stumm CL, Halcsik E, Landgraf RG, Camara NO, Sogayar MC, Jancar S. Lung remodeling in a mouse model of asthma involves a balance between TGF-beta1 and BMP-7. PLoS One 2014; 9:e95959.
3
4. Taube C, Dakhama A, Gelfand EW. Insights into the pathogenesis of asthma utilizing murine models. Int Arch Allergy Immunol 2004; 135:173-186.
4
5. Lee MY, Seo CS, Ha H, Jung D, Lee H, Lee NH, et al. Protective effects of Ulmus davidiana var. japonica against OVA-induced murine asthma model via upregulation of heme oxygenase-1. J Ethnopharmacol 2010; 130:61-69.
5
6. Richardson ET, Shukla S, Sweet DR, Wearsch PA, Tsichlis PN, Boom WH, et al. Toll-like receptor 2-dependent extracellular signal-regulated kinase signaling in Mycobacterium tuberculosis-infected macrophages drives anti-inflammatory responses and inhibits Th1 polarization of responding T cells. Infect Immun 2015; 83:2242-2254.
6
7. Liscovsky MV, Ranocchia RP, Alignani DO, Gorlino CV, Moron G, Maletto BA, et al. CpG-ODN+IFN-gamma confer pro- and anti-inflammatory properties to peritoneal macrophages in aged mice. Exp Gerontol 2011; 46:462-467.
7
8. Nguyen TH, Casale TB. Immune modulation for treatment of allergic disease. Immunol Rev 2011; 242:258-271.
8
9. Wisniewski JA, Borish L. Novel cytokines and cytokine-producing T cells in allergic disorders. Allergy Asthma Proc 2011; 32:83-94.
9
10. Vitiello L, Gorini S, Rosano G, la Sala A. Immunoregulation through extracellular nucleotides. Blood 2012; 120:511-518.
10
11. Di Virgilio F. Purines, purinergic receptors, and cancer. Cancer Res 2012; 72:5441-5447.
11
12. Aymeric L, Apetoh L, Ghiringhelli F, Tesniere A, Martins I, Kroemer G, et al. Tumor cell death and ATP release prime dendritic cells and efficient anticancer immunity. Cancer Res 2010; 70:855-858.
12
13. la Sala A, Ferrari D, Corinti S, Cavani A, Di Virgilio F, Girolomoni G. Extracellular ATP induces a distorted maturation of dendritic cells and inhibits their capacity to initiate Th1 responses. J Immunol 2001; 166:1611-1617.
13
14. Weinhold K, Krause-Buchholz U, Rodel G, Kasper M, Barth K. Interaction and interrelation of P2X7 and P2X4 receptor complexes in mouse lung epithelial cells. Cell Mol Life Sci 2010; 67:2631-2642.
14
15. Barth K, Kasper M. Membrane compartments and purinergic signalling: occurrence and function of P2X receptors in lung. Febs J 2009; 276:341-353.
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16. Wareham K, Vial C, Wykes RC, Bradding P, Seward EP. Functional evidence for the expression of P2X1, P2X4 and P2X7 receptors in human lung mast cells. Br J Pharmacol 2009; 157:1215-1224.
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17. Inoue K. The function of microglia through purinergic receptors: neuropathic pain and cytokine release. Pharmacol Ther 2006; 109:210-226.
17
18. Li F, Guo N, Ma Y, Ning B, Wang Y, Kou L. Inhibition of P2X4 suppresses joint inflammation and damage in collagen-induced arthritis. Inflammation 2014; 37:146-153.
18
19. Shi F, Zhou D, Ji Z, Xu Z, Yang H. Anti-arthritic activity of luteolin in Freund’s complete adjuvant-induced arthritis in rats by suppressing P2X4 pathway. Chem Biol Interact 2015; 226:82-87.
19
20. Zhou TT, Wu JR, Chen ZY, Liu ZX, Miao B. Effects of dexmedetomidine on P2X4Rs, p38-MAPK and BDNF in spinal microglia in rats with spared nerve injury. Brain Res 2014; 1568:21-30.
20
21. Choi JR, Lee CM, Jung ID, Lee JS, Jeong YI, Chang JH, et al. Apigenin protects ovalbumin-induced asthma through the regulation of GATA-3 gene. Int Immunopharmacol 2009; 9:918-924.
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22. Vanacker NJ, Palmans E, Kips JC, Pauwels RA. Fluticasone inhibits but does not reverse allergen-induced structural airway changes. Am J Respir Crit Care Med 2001; 163:674-679.
22
23. Chen K, Zhang J, Zhang W, Zhang J, Yang J, Li K, et al. ATP-P2X4 signaling mediates NLRP3 inflammasome activation: a novel pathway of diabetic nephropathy. Int J Biochem Cell Biol 2013; 45:932-943.
23
24. Ni X, Li X, Fang X, Li N, Cui W, Zhang B. NGF/TrkA-mediated Kidins220/ARMS signaling activated in the allergic airway challenge in mice. Ann Allergy Asthma Immunol 2010; 105:299-306.
24
25. Kim YK, Oh SY, Jeon SG, Park HW, Lee SY, Chun EY, et al. Airway exposure levels of lipopolysaccharide determine type 1 versus type 2 experimental asthma. J Immunol 2007; 178:5375-5382.
25
26. Yan L, Xiao-Ling S, Zheng-Yan C, Guo-Ping L, Sen Z, Zhuang C. HSP70/CD80 DNA vaccine inhibits airway remodeling by regulating the transcription factors T-bet and GATA-3 in a murine model of chronic asthma. Arch Med Sci 2013; 9:906-915.
26
27. Herrick CA, Das J, Xu L, Wisnewski AV, Redlich CA, Bottomly K. Differential roles for CD4 and CD8 T cells after diisocyanate sensitization: genetic control of TH2-induced lung inflammation. J Allergy Clin Immunol 2003; 111:1087-1094.
27
28. Wynn TA, Morawetz R, Scharton-Kersten T, Hieny S, Morse HC, 3rd, Kuhn R, et al. Analysis of granuloma formation in double cytokine-deficient mice reveals a central role for IL-10 in polarizing both T helper cell 1- and T helper cell 2-type cytokine responses in vivo. J Immunol 1997; 159:5014-5023.
28
29. Idzko M, Hammad H, van Nimwegen M, Kool M, Willart MA, Muskens F, et al. Extracellular ATP triggers and maintains asthmatic airway inflammation by activating dendritic cells. Nat Med 2007; 13:913-919.
29
30. Kim MJ, Turner CM, Hewitt R, Smith J, Bhangal G, Pusey CD, et al. Exaggerated renal fibrosis in P2X4 receptor-deficient mice following unilateral ureteric obstruction. Nephrol Dial Transplant 2014; 29:1350-1361.
30
31. Soto F, Garcia-Guzman M, Gomez-Hernandez JM, Hollmann M, Karschin C, Stuhmer W. P2X4: an ATP-activated ionotropic receptor cloned from rat brain. Proc Natl Acad Sci U S A 1996; 93:3684-3688.
31
32. Ravanti L, Toriseva M, Penttinen R, Crombleholme T, Foschi M, Han J, et al. Expression of human collagenase-3 (MMP-13) by fetal skin fibroblasts is induced by transforming growth factor beta via p38 mitogen-activated protein kinase. Faseb J 2001; 15:1098-1100.
32
33. Stellato C, Brummet ME, Plitt JR, Shahabuddin S, Baroody FM, Liu MC, et al. Expression of the C-C chemokine receptor CCR3 in human airway epithelial cells. J Immunol 2001; 166:1457-1461.
33
ORIGINAL_ARTICLE
Deep brain stimulation in a rat model of post-traumatic stress disorder modifies forebrain neuronal activity and serum corticosterone
Objective(s): Post-traumatic stress disorder (PTSD), one of the most devastating kinds of anxiety disorders, is the consequence of a traumatic event followed by intense fear. In rats with contextual fear conditioning (CFC), a model of PTSD caused by CFC (electrical foot shock chamber), deep brain stimulation (DBS) alleviates CFC abnormalities.Materials and Methods: Forty Male Wistar rats (220–250 g) were divided into 5 groups (n=8) and underwent stereotactic surgery to implant electrodes in the right basolateral nucleus of the amygdala (BLn). After 7 days, some animals received a foot shock, followed by another 7-day treatment schedule (DBS treatment). Next, freezing behavior was measured as a predicted response in the absence of the foot shock (re-exposure time). Blood serum corticosterone levels and amygdala c-Fos protein expression were assessed using Enzyme-linked immunosorbent assay (ELISA) and Western blot, respectively. Furthermore, freezing behaviors by re-exposure time test and general anxiety by elevated plus-maze (EPM) were evaluated. Results: PTSD decreased serum corticosterone levels and increased both amygdala c-Fos expression and freezing behaviors. Therefore, DBS treatment significantly (P<0.001) enhanced serum corticosterone levels and could significantly (P<0.001) reduce both c-Fos protein expression and freezing behaviors’ duration. However, DBS treatment has no effect on the general anxiety in PTSD rats.Conclusion: We argue that these outcomes might demonstrate the mechanism of DBS treatment, a complete therapeutic strategy, in PTSD patients.
https://ijbms.mums.ac.ir/article_10327_1d5f13133009df8cae6532276555923e.pdf
2018-04-01
370
375
10.22038/ijbms.2018.27482.6705
Amygdala
Anxiety behavior
Corticosterone
c-Fos
Deep brain stimulation
Freezing behavior
Post-traumatic stress disorder
Mina
Mokhtari hashtjini
mina_hashtjin65@yahoo.com
1
Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Gila
Pirzad Jahromi
dbspaper1395@gmail.com
2
Neuroscience Research Centre, Baqiyatallah University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Seyed Shahabeddin
sadr
shahabsadr2002@yahoo.com
3
Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Gholam Hossein
Meftahi
meftahi208@yahoo.com
4
Neuroscience Research Centre, Baqiyatallah University of Medical Sciences, Tehran, Iran
AUTHOR
Boshra
Hatef
boshrahatef@yahoo.com
5
Neuroscience Research Centre, Baqiyatallah University of Medical Sciences, Tehran, Iran
AUTHOR
Danial
Javidnazar
dan_javid@yahoo.com
6
Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
1. Langevin J-P, De Salles AAF, Kosoyan HP, Krahl SE. Deep brain stimulation of the amygdala alleviates post-traumatic stress disorder symptoms in a rat model. J Psychiatr Res 2010; 44:1241-1245.
1
2. Delgado MR, Olsson A, Phelps EA. Extending animal models of fear conditioning to humans. Biol Psychol 2006; 73:39-48.
2
3. Milad MR, Rauch SL, Pitman RK, Quirk GJ. Fear extinction in rats: implications for human brain imaging and anxiety disorders. Biol Psychol 2006; 73:61-71.
3
4. Yehuda R, LeDoux J. Response variation following trauma: a translational neuroscience approach to understanding PTSD. Neuron 2007; 56:19-32.
4
5. Shin LM, Wright CI, Cannistraro PA, Wedig MM, McMullin K, Martis B, et al. A functional magnetic resonance imaging study of amygdala and medial prefrontal cortex responses to overtly presented fearful faces in posttraumatic stress disorder. Archives of general psychiatry 2005; 62:273-281.
5
6. Shin LM, Orr SP, Carson MA, Rauch SL, Macklin ML, Lasko NB, et al. Regional cerebral blood flow in the amygdala and medial prefrontal cortex during traumatic imagery in male and female Vietnam veterans with PTSD. Archives of general psychiatry. 2004; 61:168-176.
6
7. Protopopescu X, Pan H, Tuescher O, Cloitre M, Goldstein M, Engelien W, et al. Differential time courses and specificity of amygdala activity in posttraumatic stress disorder subjects and normal control subjects. Biological psychiatry. 2005; 57: 464-473.
7
8. Yehuda R. Status of Glucocorticoid Alterations in Post‐traumatic Stress Disorder. Annals of the New York Academy of Sciences 2009; 1179:56-69.
8
9. Franzini A, Broggi G, Cordella R, Dones I, Messina G. Deep-brain stimulation for aggressive and disruptive behavior. World neurosurgery 2013; 80:S29 e11-4.
9
10. Marin MF, Camprodon JA, Dougherty DD, Milad MR. Device‐based brain stimulation to augment fear extinction: implications for ptsd treatment and beyond. Depression and anxiety. 2014; 31:269-278.
10
11. Stidd DA, Vogelsang K, Krahl SE, Langevin J-P, Fellous J-M. Amygdala Deep Brain Stimulation Is Superior to Paroxetine Treatment in a Rat Model of Posttraumatic Stress Disorder. Brain Stimulation: Basic, Translational, and Clinical Research in Neuromodulation 2013; 6:837-844.
11
12. Rosa M, Giannicola G, Marceglia S, Fumagalli M, Barbieri S, Priori A. Neurophysiology of deep brain stimulation. Int Rev Neurobiol 2012; 107:23-55.
12
13. de Koning PP, Figee M, Endert E, Storosum JG, Fliers E, Denys D. Deep brain stimulation for obsessive–compulsive disorder is associated with cortisol changes. Psychoneuroendocrinology 2013; 38:1455-1459.
13
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21. Asalgoo S, Tat M, Sahraei H, Pirzad G. Crocin as a psychoactive agent can be target regulation of Hypothalamic-Pituitary-Adrenal axis activity. Frontiers in Neuroscience 2017; 11:668.
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23. Sahraei H, Fatahi Z, Eidi A, Haeri-Rohani A, Hooshmandi Z, Shekarforoush S, et al. Inhibiting Post Traumatic Stress Disorder (PTSD) induced by electric shock using ethanol extract of saffron in rats. J Biol Res Thessalon 2012;18:320-327.
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25. Frances Davies M, Tsui J, Flannery JA, Li X, DeLorey TM, Hoffman BB. Activation of [alpha]2 Adrenergic Receptors Suppresses Fear Conditioning: Expression of c-Fos and Phosphorylated CREB in Mouse Amygdala. Neuropsychopharmacology 2003; 29:229-239.
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37
ORIGINAL_ARTICLE
Evaluation of nicotinic receptor of pedunculopontine tegmental nucleus in central cardiovascular regulation in anesthetized rat
Objective(s): Cholinergic neurons are important neurons in the Pedunculopontine tegmental nucleus (PPT). In this study, nicotinic receptor of the PPT in central cardiovascular regulation in the anesthetized rat was evaluated. Materials and Methods: Saline, acetylcholine (Ach; doses: 90 and 150 nmol), hexamethonium (Hexa; doses: 100 and 300 nmol) and higher doses of Hexa (300 nmol) + Ach (150 nmol) microinjected into the PPT. The femoral artery was cannulated and cardiovascular responses were continuously recorded by a power lab system. After injection of drugs, peak changes of mean arterial pressure (∆MAP), systolic blood pressure (∆SBP) and heart rate (∆HR) calculated and compared with saline group.Results: The ∆SBP and ∆MAP significantly decreased by two doses of Ach (PConclusion: These results indicate that nicotinic receptor of the PPT has an inhibitory effect on ∆HR with no significant effect on ∆MAP or ∆SBP.
https://ijbms.mums.ac.ir/article_10366_c9fa77f5039c35fd19ef5141514bcdf3.pdf
2018-04-01
376
381
10.22038/ijbms.2018.25616.6319
Acetylcholine
Blood pressure Hexamethonium
Nicotinic receptor
Pedunculopontine tegmental nucleus
Tahereh
Nikyar
nikyar1988@gmail.com
1
Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mahmoud
Hosseini
hosseinim@mums.ac.ir
2
Division of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Saeed
Niazmand
niazmands@mums.ac.ir
3
Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mohammad Naser
Shafei
shafeimn@mums.ac.ir
4
Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
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20. Dai YWE, Lee YH, YS Chen J, Lin YK, Hwang LL. Expression of the M3 Muscarinic Receptor on Orexin Neurons that Project to the Rostral Ventrolateral Medulla. Anat Rec 2016; 299:660-668.
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25. Le Novere N, Corringer PJ, Changeux JP. The diversity of subunit composition in nAChRs: evolutionary origins, physiologic and pharmacologic consequences. J Neurobiol 2002; 53:447-456.
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26. Matsuyama S, Matsumoto A. Epibatidine induces long-term potentiation (LTP) via activation of. ALPHA. 4. BETA. 2 nicotinic acetylcholine receptors (nAChRs) in vivo in the intact mouse dentate gyrus: both. ALPHA. 7 and. ALPHA. 4. BETA. 2 nAChRs essential to nicotinic LTP. J Pharmacol Sci 2003; 93:180-187.
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47
ORIGINAL_ARTICLE
Can crocin play a preventive role in Wistar rats with carbon tetrachloride-induced nephrotoxicity?
Objective(s): To investigate protective role of crocin by attempting to create nephrotoxicity with carbon tetrachloride.Materials and Methods: Ethics committee approval was obtained and 50 male Wistar rats were randomly divided into 5 groups that included 10 rats each: Control, Corn oil, Crocin, Carbon tetrachloride (CCl4), and Crocin + Carbon tetrachloride. Following the experiments, the rats were decapitated under anesthesia and incised kidney tissues were subjected to biochemical and histological examinations.Results: In the CCl4 administered group, MDA, TOS, Bun, and creatinine levels increased, GSH, SOD, CAT, and TAS levels decreased (P≤0.05), glomerular collapse in kidney sections, narrowing and local occlusion in Bowman’s space in certain glomeruli, inflammatory cell infiltration and congestion were observed when compared to all other groups. There was a significant decrease in increased MDA, TOS, Bun, and creatinine levels, and a significant increase in decreased GSH, SOD, CAT, and TAS levels in CCl4 + crocin administered group compared to the CCl4 group (P≤0.05), local minimal glomerular damage, tubular damage, inflammatory infiltration, and vascular collagen symptoms were observed in kidney sections, however significant improvement was observed in damage findings when compared to the CCl4 group.Conclusion: At this dose and time interval, against a highly toxic chemical such as CCl4, crocin was able to suppress oxidative stress by playing a protective role in the kidney tissue.
https://ijbms.mums.ac.ir/article_10333_fed90f7ed0737a95d9b4997bef402d51.pdf
2018-04-01
382
387
10.22038/ijbms.2018.26101.6412
Crocin
Carbon tetrachloride
Kidney
Oxidative stress
Rat
Mehmet
Erdemli
ermanerdemli@hotmail.com
1
Department of Medical Biochemistry, Medical Faculty, Nigde Omer Halisdemir University, Nigde, Turkey
LEAD_AUTHOR
Mehmet
Gul
2
Department of Histology and Embryology, Medical Faculty, Inonu University, Malatya, Turkey
AUTHOR
Eyup
Altinoz
eyupaltinoz@karabuk.edu.tr
3
Department of Medical Biochemistry, Medical Faculty, Karabuk University, Karabuk, Turkey
AUTHOR
Zeynep
Aksungur
zeynepaksungur.44@gmail.com
4
Department of Medical Biochemistry, Medical Faculty, Inonu University, Malatya, Turkey
AUTHOR
Semir
Gul
5
Department of Histology and Embryology, Medical Faculty, Inonu University, Malatya, Turkey
AUTHOR
Harika
Bag
6
Department of Biostatistics, Medical Faculty, Inonu University, Malatya, Turkey
AUTHOR
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42
ORIGINAL_ARTICLE
Development of monoclonal antibodies against axenic amastigotes of Leishmania infantum strain in Iran: Implication for diagnosis of Kala-azar
Objective(s): Leishmaniasis is endemic in 88 countries. Amastigote forms of Leishmania are experts at exploiting host cell processes to establish infection. Monoclonal antibodies are key reagents used in the diagnosis of infectious and non-infectious diseases. The aim of this study was to produce monoclonal antibodies against axenic amastigotes of the Leishmania infantum strain in Iran.Materials and Methods: First, standard strains were cultured and axenic amastigote antigens of L. infantum were obtained. Since then, BALB/c mice were immunized and antibody titers were determined. For hybridoma cell formation, lymphocytes isolated from spleen of immunized mice and myeloma cells were fused at a ratio of 10 to 1 in the presence of polyethylene glycol, followed by limiting dilution for the isolation of monoclones. Subsequently, antibody isotypes were determined by using the isotyping kit. The best clone was injected intraperitoneally to pristane-primed mice for large scale production of monoclonal antibodies. The specificity of antibody was determined with Western blotting.Results: Approximately 25 positive monoclones were obtained, of which four hybrids producing anti-amastigotes L. infantum monoclonal antibodies with high optical density (OD), selected and designated as 8D2 FVI6, 8D2 FVI3, 6G2 FV4 and 6G2 FV3. Results from isotype determination showed the IgG2b sub-class in 6G2FV2 and 8D2FVI6 monoclones. Conclusion: This study produced monoclonal antibody against amastigotes of Iranian strain of L. infantum for the first time. These antibodies have reactivity against Iranian strain of L. infantum and can be used in the diagnosis of Kala-azar.
https://ijbms.mums.ac.ir/article_10325_0e5a15dd285e3fe17d223f34d56d23f5.pdf
2018-04-01
388
394
10.22038/ijbms.2018.25355.6264
Axenic amastigotes
Hybridoma cells
Leishmaniases
Leishmania infantum
Monoclonal antibodies
Ezzat
nourizadeh
nourizade@ut.ac.ir
1
School of Biology, College of Science, University of Tehran, Tehran, Iran
AUTHOR
Seyed Jalal
Zargar
zargar@ut.ac.ir
2
School of Biology, College of Science, University of Tehran, Tehran, Iran
LEAD_AUTHOR
Mohammad Hossein
Alimohammadian
mhalimoham@gmail.com
3
Department of Immunology, Pasteur Institute of Iran, Tehran, Iran
AUTHOR
Soheila
Ajdary
sohary@yahoo.com
4
Department of Immunology, Pasteur Institute of Iran, Tehran, Iran
AUTHOR
Mehdi
Mahdavi
mahdavivac@gmail.com
5
Department of Immunology, Pasteur Institute of Iran, Tehran, Iran
AUTHOR
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27. Sereno D, Cavaleyra M, Zemzoumi K, Maquaire S , Ouaissi A, Lemesre JL. Axenically grown amastigotes of Leishmania infantum used as an In vitro model to investigate the pentavalent antimony mode of action. Antimicrob Agents Chemother 1998;42: 3097–3102.
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28. Kurtzhals JAL, Hey AS, Jardim A, Kemp M, Schaefer KU, Odera EO, Christensen CBV, Githure JI, Olafson RW, Theander TG, Kharazmi A. Dichotomi of the human T cell response to Leishmania antigens. II. Absent or Th2-like response to gp63 and Th1-like response to lipophosphoglycan-associated protein in cells from cured visceral leishmaniasis patients. Clin Exp Immunol 1994;96: 416-421.
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50
ORIGINAL_ARTICLE
The effect of intracerebroventricular injection of CGRP on pain behavioral responses and monoamines concentrations in the periaqueductal gray area in rat
Objective(s): Calcitonin gene related peptide (CGRP) receptors are widely distributed in the central nervous system. The aim of this study was to investigate the effects of intracerebroventricular (ICV) injection of CGRP on pain behavioral responses and on levels of monoamines in the periaqueductal gray area (PAG) during the formalin test in rats.Materials and Methods: Twenty-four male rats were studied in four groups (n=6). CGRP was injected into the left cerebral ventricle (1.5 nmol, 5 µl). After 20 min, formalin (2.5%) was subcutaneously injected into the right hind paw. Behavior nociceptive score was recorded up to 60 min. During the formalin test, the PAG was subjected to microdialysis and levels of norepinephrine, 3-methoxy-4-hydroxyphenyl-glycol (HMPG), dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), serotonin and 5-hydroxyindole-acetic acid (HIAA) were measured by HPLC.Results: ICV injection of CGRP lead to a significant pain reduction in acute, middle and chronic phases of the formalin test. Dialysate concentrations of norepinephrine, HMPG, dopamine, DOPAC, serotonin and HIAA in the PGA area showed an increase in acute phase, middle phase and beginning of the chronic phase of the formalin test.Conclusion: CGRP significantly reduced pain by increased concentrations of monoamines and their metabolites in dialysates from PAG when injected ICV to rats.
https://ijbms.mums.ac.ir/article_10326_9e774992f846e1aafd76e1595bd0844c.pdf
2018-04-01
395
399
10.22038/ijbms.2018.26384.6467
CGRP
Formalin test
HPLC
Monoamines
Microdialysis
Kaveh
Rahimi
kaveh_rahimi66a@yahoo.com
1
Department of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran
AUTHOR
Javad
Sajedianfard
sajedian@shirazu.ac.ir
2
Department of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran
LEAD_AUTHOR
Ali Akbar
Owji
owjiaa@sums.ac.ir
3
Department of Basic Sciences,, School of Medicine, Shiraz University of Medical Sciences, Shiraz,Iran
AUTHOR
1. Vanegas H, Schaible H-G. Descending control of persistent pain: inhibitory or facilitatory? Brain Res Rev 2004; 46:295-309.
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2. Fields HL BA, Heinricher MM. Central nervous system mechanisms of pain modulation. In: McMahon S, Koltzenburg M, eds Textbook of Pain Burlington, Massachusetts, USA: Elsevier Health Sciences. 2005;5th ed:125-142.
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3. Bourgeais L, Monconduit L, Villanueva L, Bernard JF. Parabrachial internal lateral neurons convey nociceptive messages from the deep laminas of the dorsal horn to the intralaminar thalamus. J Neurosci Res 2001; 21:2159-2165.
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4. Bannister K, Dickenson AH. What do monoamines do in pain modulation? Curr Opin Support Palliat Care 2016; 10:143-148.
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5. Kwiat GC, Basbaum AI. Organization of tyrosine hydroxylase- and serotonin-immunoreactive brainstem neurons with axon collaterals to the periaqueductal gray and the spinal cord in the rat. Brain Res 1990; 528:83-94.
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6. Durham PL, Vause CV. Calcitonin gene-related peptide (CGRP) receptor antagonists in the treatment of migraine. CNS drugs 2010; 24:539-548.
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7. Ho TW, Edvinsson L, Goadsby PJ. CGRP and its receptors provide new insights into migraine pathophysiology. Nat Rev Neurol 2010; 6:573-582.
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8. Sexton PM, McKenzie JS, Mendelsohn FA. Evidence for a new subclass of calcitonin/ calcitonin gene-related peptide binding site in rat brain. Neurochem int 1988; 12:323-335.
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9. Henke H, Tschopp FA, Fischer JA. Distinct binding sites for calcitonin gene-related peptide and salmon calcitonin in rat central nervous system. Brain Res 1985; 360:165-171.
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11. Kruger L, Mantyh PW, Sternini C, Brecha NC, Mantyh CR. Calcitonin gene-related peptide (CGRP) in the rat central nervous system: patterns of immunoreactivity and receptor binding sites. Brain Res 1988; 463:223-244.
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12. Sexton PM. Central nervous system binding sites for calcitonin and calcitonin gene-related peptide. Mol Neurobiol 1991; 5:251-273.
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13. Walker CS, Hay DL. CGRP in the trigeminovascular system: a role for CGRP, adrenomedullin and amylin receptors? Br J Pharmacol 2013; 170:1293-1307.
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14. Pozo-Rosich P, Storer RJ, Charbit AR, Goadsby PJ. Periaqueductal gray calcitonin gene-related peptide modulates trigeminovascular neurons. Cephalalgia: Cephalalgia 2015; 35:1298-1307.
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15. Storer RJ, Akerman S, Goadsby PJ. Calcitonin gene-related peptide (CGRP) modulates nociceptive trigeminovascular transmission in the cat. Br j pharmacol 2004; 142:1171-1181.
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18. G Paxinos CW. The Rat Brain in Stereotaxic Coordinates. 6th, editor. Sydney: Academic Press; 2006.
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20. Coderre TJ, Fundytus ME, McKenna JE, Dalal S, Melzack R. The formalin test: a validation of the weighted-scores method of behavioural pain rating. Pain 1993; 54:43-50.
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21. Gebhart GF. Descending modulation of pain. Neurosci Biobehav Rev 2004; 27:729-737.
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22. Ossipov MH, Dussor GO, Porreca F. Central modulation of pain. J Clin Invest 2010; 120:3779-3787.
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23. Garcia-Ramirez DL, Calvo JR, Hochman S, Quevedo JN. Serotonin, dopamine and noradrenaline adjust actions of myelinated afferents via modulation of presynaptic inhibition in the mouse spinal cord. PloS One 2014; 9:189-199.
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24. Huang Y, Brodda-Jansen G, Lundeberg T, Yu LC. Anti-nociceptive effects of calcitonin gene-related peptide in nucleus raphe magnus of rats: an effect attenuated by naloxone. Brain Res 2000; 873:54-59.
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25. Su HC, Wharton J, Polak JM, Mulderry PK, Ghatei MA, Gibson SJ, et al. Calcitonin gene-related peptide immunoreactivity in afferent neurons supplying the urinary tract: combined retrograde tracing and immunohistochemistry. J Neurosci Res 1986; 18:727-747.
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26. Harmann PA, Chung K, Briner RP, Westlund KN, Carlton SM. Calcitonin gene-related peptide (CGRP) in the human spinal cord: a light and electron microscopic analysis. The J Comp Neurol 1988; 269:371-380.
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27. Poyner DR. Calcitonin gene-related peptide: multiple actions, multiple receptors. Pharmacol Ther 1992; 56:23-51.
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28. Dobolyi A, Irwin S, Makara G, Usdin TB, Palkovits M. Calcitonin gene-related peptide-containing pathways in the rat forebrain. J Comp Neurol 2005; 489:92-119.
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29. Seybold VS. The role of peptides in central sensitization. Handb Exp Pharmacol 2009:451-491.
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30. Sprenger T, Goadsby PJ. Migraine pathogenesis and state of pharmacological treatment options. BMC Med 2009; 7:65-76.
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31. Khoshdel Z, Takhshid MA, Owji AA. Intrathecal Amylin and Salmon Calcitonin Affect Formalin Induced c-Fos Expression in the Spinal Cord of Rats. Iran J Med Sci 2014; 39:543-551.
31
32. Cridland RA, Henry JL. Effects of intrathecal administration of neuropeptides on a spinal nociceptive reflex in the rat: VIP, galanin, CGRP, TRH, somatostatin and angiotensin II. Neuropeptides 1988; 11:23-32.
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33. Yu L-C, Weng X-H, Wang J-W, Lundeberg T. Involvement of calcitonin gene-related peptide and its receptor in anti-nociception in the periaqueductal grey of rats. Neurosci Lett 2003; 349:1-4.
33
34. Walker CS, Conner AC, Poyner DR, Hay DL. Regulation of signal transduction by calcitonin gene-related peptide receptors. Trends Pharmacol Sci 2010; 31:476-483.
34
ORIGINAL_ARTICLE
Association between biofilm production, adhesion genes and drugs resistance in different SCCmec types of methicillin resistant Staphylococcus aureus strains isolated from several major hospitals of Iran
Objective(s): The ability of bacteria to produce biofilm and adhesion makes them more resistant to antibiotics. The current study aims to evaluate the biofilm formation by Staphylococcus aureus and to determine the prevalence of adhesion genes, also their correlation with drug resistance.Materials and Methods: A total of 96 MRSA were collected from hospitals of Iran’s western provinces during 2012 to 2013. The presence of ica A,B,C,D,clfA, cna, fnbA, mecA genes were determined by PCR technique. Biofilm formation was studied by microtiter plate assay, the clonal relations of the strains were examined by SCCmec and Spa typing. Results: The results demonstrated that 96 % of isolates were biofilm producers. The distributions of biofilm formation between isolates were 4.2%, 54.2%, 35.4% as high, moderate and weak, respectivelly. The highest biofilm production was observed from blood culture isolates. All virulent genes ica A,B,C,D,clfA, cna, fnbA were observed in moderate and weak biofilm formation isolates. Among high biofilm formation isolates, icaB and cna genes were not seen. Statistical analysis showed that there was a significant correlation between ica, fnbA and the biofilm production, but there was not a significant correlation between the type of samples and drug resistance, spa type and SCCmec type with biofilm production (P>0.05). Frequency of All virulent genes in type III SCCmec was higher than other types. Conclusion: The majority of MRSA isolates were biofilm producers and blood isolates ranked as the great biofilm producer. In these isolates ica D and fnbA genes are correlated with biofilm production.
https://ijbms.mums.ac.ir/article_10463_22e8a3fd35b0231b705e2221ec4394f6.pdf
2018-04-01
400
403
10.22038/ijbms.2018.19378.5132
Antiseptic
Biofilm
MRSA
Resistance genes qacA/B
Lida
Bimanand
1
Clinical Microbiology Research Center, Ilam University of Medical Sciences, Ilam, Iran
AUTHOR
Morovat
Taherikalani
taherikalani@gmail.com
2
Clinical Microbiology Research Center, Ilam University of Medical Sciences, Ilam, Iran
AUTHOR
Farid
Azizi Jalilian
azizifarid@gmail.com
3
Clinical Microbiology Research Center, Ilam University of Medical Sciences, Ilam, Iran
AUTHOR
Nourkhoda
Sadeghifard
4
Clinical Microbiology Research Center, Ilam University of Medical Sciences, Ilam, Iran
AUTHOR
Sobhan
Ghafourian
5
Clinical Microbiology Research Center, Ilam University of Medical Sciences, Ilam, Iran
AUTHOR
Zahra
Mahdavi
6
Clinical Microbiology Research Center, Ilam University of Medical Sciences, Ilam, Iran
AUTHOR
Sattar
Mohamadi
7
Clinical Microbiology Research Center, Ilam University of Medical Sciences, Ilam, Iran
AUTHOR
Kouresh
Sayehmiri
8
Department of Biostatistic, Faculty of Medicine, Ilam University of Medical Sciences, Ilam/ Iran
AUTHOR
Ali
Hematian
9
Department of Microbiology, Faculty of Medicine, Ilam University of Medical Sciences, Ilam/ Iran
AUTHOR
Iraj
Pakzad
pakzad_i2006@yahoo.com
10
Clinical Microbiology Research Center, Ilam University of Medical Sciences, Ilam, Iran
LEAD_AUTHOR
1. Hoyle BD, JW. Costerton. Bacterial resistance to antibiotics: the role of biofilms. Prog Drug Res 1991; 37:91–105.
1
2. Yazdani R, Oshaghi M, Havayi A, Salehi R, Sadeghizadeh M, Foroohesh H. Detection of icaAD gene and biofilm formation in Staphylococcus aureus isolates from wound infections. Iranian J Publ Health 2006; 35: 25-28.
2
3. Ammendolia MG, Rosa RD, Montanaro L, Arciola CR and Baldassarri L. Slime production and expression of slime–associated antigen by staphylococcal clinical isolates. J Clin Microbiol 1999; 37: 3235–3238.
3
4. OGara JP, Humphreys H. Staphylococcus epidermidis biofilms importance and implications. H Med Microbiol 2001; 50: 582-587.
4
5. Nathan KA, Mark JM, Costerton JV, Leid JG, Powers ME, Shirtliff ME. Staphylococcus aureus biofilms. Virulence 2011; 2: 445–459.
5
6. Cucarella C, Tormo MA, Ubeda C, Trotonda MP, Monzón M, Peris C. Role of biofilm-associated protein bap in the pathogenesis of bovine Staphylococcus aureus. Infect. Immun 2004; 72: 2177–2185.
6
7. Clinical and Laboratory Standards Institute (CLSI). CLSI document M100-S24. Wayne, PA: Clinical and Laboratory Standards Institute 2015.
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8. Francois P, Vaudaux P, Foster TJ, Lew DP. Host-bacteria interactions in foreign body infections. Infect Control Hosp Epidemiol 1996;17: 514–520.
8
9. Montanaro L, Arciola CR, Borsetti E, Brigotti M, Baldassarri L. A polymerase chain reaction (PCR) method for the identification of collagen adhesin gene (cna) in Staphylococcus-induced prosthesis infections. New Microbiol 1998;21: 359–363.
9
10. Cramaton, SE, Gerke C, Gotz F. In-vitro method to study Staphylococcal biofilm formation. Methods Enzymol 2001; 336: 239-55.
10
11. Arciola, CR, Baldassarri L, Montanaro L. Presence of icaA and icaD genes and slime production in a collection of Staphylococcal strains from catheterassociated infections. J Clin Microbiol 2001;39: 2151 -2156.
11
12. Serray B, Oufrid S, Hannaoui I, Bourjilate F, Soraa N, Mliji M, et al. Genes encoding adhesion factors and biofilm formation in methicillin-resistant Staphylococcus aureus in Morocco. J Infect Dev Ctries 2016; 10: 863-9.
12
13. Halebeedu Prakash P, Rajan V, Gopal S. Predominance of SCCmec types IV and V among biofilm producing device-associated Staphylococcus aureus strains isolated from tertiary care hospitals in Mysuru, India. Enferm Infecc Microbiol Clin 2017; 35: 229-235.
13
ORIGINAL_ARTICLE
The protective effects of naringin against 5-fluorouracil-ınduced hepatotoxicity and nephrotoxicity in rats
Objective(s): 5-FU, an anticarcinogenic agent, is reported to have side-effects that include hepatotoxicity and nephrotoxicity. The study objective was to investigate the protective effects of naringin on 5-FU-induced hepatotoxicity and nephrotoxicity.Materials and Methods: Thirty rodents were assigned to three groups. The control group received 1 ml of intragastric distilled water for 14 days. The 5-FU group received 1 ml of distilled water for 14 days as a placebo. On day 9, this same group received a 20 mg/kg dose of 5-FU administered intraperitoneally(IP) for a further five days. The naringin+5-FU group received a 100 mg/kg dose of naringin (IP) for 14 days. On day 9, 20 mg/kg of 5-FU was administered (IP) to this group for a further five days. On day 15, the rats were decapitated, and blood and renal and hepatic tissues were taken.Results: It was determined that serum creatinine, BUN, AST, ALT, ALP, and LDH levels, as well as cytokine levels in the liver and kidney tissues were significantly elevated in the 5-FU group, compared to the control group. The comparative values were similar in the control and naringin+5-FU groups. When the liver tissue was examined histopathologically, in the control group it was found to be normal in structure. However, necrosis was observed in the hepatocytes of the pericentric region in the 5-FU group. 8-OHdG cell density was significantly elevated in the 5-FU group, compared to the control and naringin+5-FU groups.Conclusion: Naringin was observed to have a protective effect on 5-FU-induced liver and kidney damage.
https://ijbms.mums.ac.ir/article_10374_a30ca0284f97e03c598d19489f39a645.pdf
2018-04-01
404
410
10.22038/ijbms.2018.27510.6714
5-fluorouracil
Hepatotoxicity
Naringin
Nephrotoxicity
Rat
Volkan
Gelen
gelen_volkan@hotmail.com
1
Department of Physiology, Veterinary Faculty, Kafkas University, Kars, Turkey
LEAD_AUTHOR
Emin
Şengül
gozdemirci@gmail.com
2
Department of Physiology, Veterinary Faculty, Ataturk University, Erzurum, Turkey
AUTHOR
Serkan
Yıldırım
gokhan__36@hotmail.com
3
Department of Pathology, Veterinary Faculty, Ataturk University, Erzurum, Turkey
AUTHOR
Gözde
Atila
demetdemirci331@gmail.com
4
Department of Physiology, Veterinary Faculty, Kafkas University, Kars, Turkey
AUTHOR
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49
ORIGINAL_ARTICLE
DNA protection, antioxidant and xanthin oxidase inhibition activities of polyphenol-enriched fraction of Berberis integerrima Bunge fruits
Objective(s): The aim of this study was to prepare fraction and determine the biological activities of the polyphenol-enriched fraction of Berberis integerrima Bunge fruits. Materials and Methods: In this assay fraction was extracted by column chromatography, using Amberlite column as the stationary phase. Phenol and flavonoids in the extract and fraction were analyzed by high performance liquid chromatography (HPLC). DNA protection ability, antioxidant and xanthin oxidase inhibition capacities of this fraction were also examined.Results: Phenol and flavonoid content measurement and HPLC analyses of this fraction confirmed that phenol and flavonoids were increased in fraction in comparison to extract (before using Amberlite column). In antioxidant measurement assay, the trolox equivalent values were 1.05± 0.04 and 0.8±0.11 in oxygen radical absorbance capacity (ORAC) and the EC50 values for cellular antioxidant activity were 55.51±0.21 and 95.67±0.13 µg/ml for quercetin and the fraction, respectively. The xanthin oxidase inhibition percentages were 97.6±0.003 and 90.2 6±0.003 in 100 µg/ml concentration of fraction and Vitamin C respectively. Comet assay analysis showed that this fraction protects human lymphocytes against H2O2-induced DNA damages at 12.5 to 100 µg/ml concentrations. Conclusion: This study suggests that Amberlite column as the stationary phase help to improve phenolic compound in separating fractions. The results showed that B. integerrima fruits are rich in phenolic compounds and they are potent antioxidants with protective effects on oxidative damages. They might be used as functional ingredients in food and supplements.
https://ijbms.mums.ac.ir/article_10331_ef722b2cd2686220e8bcc41d8c0e21a3.pdf
2018-04-01
411
416
10.22038/ijbms.2018.26563.6506
Antioxidant activity
Berberis integerrima Bunge
Comet assay
DNA protection
Xanthin oxidase inhibitor
Zahra
Sabahi
sabahiz@sums.ac.ir
1
Medicinal Plants Processing Research Center, Shiraz University of Medical Sciences, Shiraz, Fars, Iran
AUTHOR
Fatemeh
Farmani
fa_farmani@yahoo.com
2
Medicinal Plants Processing Research Center, Shiraz University of Medical Sciences, Shiraz, Fars, Iran
AUTHOR
Fatemeh
Soltani
soltanif@mums.ac.ir
3
Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Khorasan Razavi, Iran
AUTHOR
Mahmoodreza
Moein
mrmoein@sums.ac.ir
4
Medicinal Plants Processing Research Center, Shiraz University of Medical Sciences, Shiraz, Fars, Iran
LEAD_AUTHOR
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1
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40
ORIGINAL_ARTICLE
Effect of maternal fluoxetine exposure on lung, heart and kidney development in rat neonates
Objective(s): Depression during pregnancy negatively affects fetal development. Fluoxetine as a selective serotonin reuptake inhibitor (SSRIs) is used for treatment of gestational depression. This study is trying to determine the effects of fluoxetine on the renal, heart and lung development.Materials and Methods: Fifteen pregnant rats were treated with fluoxetine at 7 mg/kg from days 0 to 21 of gestation. Immediately after born, heart and kidney samples were evaluated for genes expression and histological assessment. Lung sample were fixed for immunohistochemical study.Results: The gene expression of BMP7 and WNT4 were reduced in the kidney of fluoxetine-treated group (P-value<0.05), but in the heart of both groups no significant difference was found in gene expression (P-value>0.05). Histological assessment showed that the glomeruli of the kidneys in treated group are more primordial compared to control. There was a developmental deficiency in Bowman’s capsule, and the capsular space was not clear. The arrangements of the filaments, the position of the nucleus and cells morphology were normal in the hearts of both groups. Immunohistochemical analysis demonstrated that in the fluoxetine-exposed group HoxB5 is more expressed in the mesenchymal cells, but in the control group the expression is limited to alveolar cells.Conclusion: According to developmental changes in kidney, heart and lung, fluoxetine affects neonatal growth during pregnancy, which may lead to delay of some organs growth. So, it is essential to survey the roles of antidepressant drugs on fatal and neonatal development during pregnancy.
https://ijbms.mums.ac.ir/article_10365_da69f2e18f7ee4c7f21f33569bea2a26.pdf
2018-04-01
417
421
10.22038/ijbms.2018.27203.6650
Fluoxetine
Heart
Kidney
Lung
SSRIs
Razieh
Taghizadeh Ghvamabadi
r_taghizade_bio@yahoo.com
1
Department of Anatomy, School of Medicine; Physiology-Pharmacology Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
AUTHOR
Zahra
Taghipour
taghipourz@yahoo.com
2
Department of Anatomy, School of Medicine; Physiology-Pharmacology Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
LEAD_AUTHOR
Mahsa
Hasanipoor
mhasanipoor@gmail.com
3
Department of Physiology-Pharmacology, School of Medicine; Physiology-Pharmacology Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
AUTHOR
Marzieh
Khademi
m.khadem6969@gmail.com
4
Department of Anatomy, School of Medicine; Physiology-Pharmacology Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
AUTHOR
Mehdi
Shariati
shariatik@gmail.com
5
Department of Anatomy, School of Medicine; Physiology-Pharmacology Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
AUTHOR
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4. Chatillon O, Even C. [Antepartum depression: prevalence, diagnosis and treatment]. Encephale 2010; 36:443-451.
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6. Moses-Kolko EL, Bogen D, Perel J, Bregar A, Uhl K, Levin B, et al. Neonatal signs after late in utero exposure to serotonin reuptake inhibitors: literature review and implications for clinical applications. JAMA 2005; 293:2372-2383.
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7. Costei AM, Kozer E, Ho T, Ito S, Koren G. Perinatal outcome following third trimester exposure to paroxetine. Arch Pediatr Adolesc Med 2002; 156:1129-1132.
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8. Kallen B. Neonate characteristics after maternal use of antidepressants in late pregnancy. Arch Pediatr Adolesc Med 2004; 158:312-316.
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13. Wang S, Yang L, Wang L, Gao L, Xu B, Xiong Y. Selective Serotonin Reuptake Inhibitors (SSRIs) and the Risk of Congenital Heart Defects: A Meta-Analysis of Prospective Cohort Studies. J Am Heart Assoc 2015; 4:e001681.
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14. Malm H, Artama M, Gissler M, Ritvanen A. Selective serotonin reuptake inhibitors and risk for major congenital anomalies. Obstet Gynecol 2011; 118:111-120.
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16. Matsumoto H. Hyponatremia associated with selective serotonin reuptake inhibitors. Intern Med 2005; 44:173-174.
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17. Shakibaei F, Gholamrezaei A, Alikhani M, Talaeizadeh K. Serum sodium changes in fluoxetine users at different age groups. Iran J Psychiatry 2010; 5:113-116.
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18. Viramontes TS, Truong H, Linnebur SA. Antidepressant-Induced Hyponatremia in Older Adults. Consult Pharm 2016; 31:139-150.
18
19. Carvalho AF SM, Brunoni AR, Vieta E, Fava GA. The safety, tolerability and risks associated with the use of newer generation antidepressant drugs: a critical review of the literature. Psychother Psychosom 2016; 85:270-288.
19
20. Girault C, Richard JC, Chevron V, Goulle JP, Droy JM, Bonmarchand G, et al. Syndrome of inappropriate secretion of antidiuretic hormone in two elderly women with elevated serum fluoxetine. J Toxicol Clin Toxicol 1997; 35:93-95.
20
21. ten Holt WL, van Iperen CE, Schrijver G, Bartelink AK. Severe hyponatremia during therapy with fluoxetine. Arch Intern Med 1996; 156:681-682.
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22. Verbalis JG. Disorders of body water homeostasis. Best Pract Res Clin Endocrinol Metab 2003; 17:471-503.
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23. Moyses ZP, Nakandakari FK, Magaldi AJ. Fluoxetine effect on kidney water reabsorption. Nephrol Dial Transplant 2008; 23:1173-1178.
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24. Taghizadeh R, Taghipour Z, Karimi A, Shamsizadeh A, Taghavi MM, Shariati M, et al. The expression of HoxB5 and SPC in neonatal rat lung after exposure to fluoxetine. Drug Des Devel Ther 2016; 10:3323-3329.
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25. Zhu H. Forkhead box transcription factors in embryonic heart development and congenital heart disease. Life Sci 2016; 144:194-201.
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26. Palmer RE, Kotsianti A, Cadman B, Boyd T, Gerald W, Haber DA. WT1 regulates the expression of the major glomerular podocyte membrane protein Podocalyxin. Curr Biol 2001; 11:1805-1809.
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28. Schmittgen TD, Livak KJ. Analyzing real-time PCR data by the comparative C(T) method. Nat Protoc 2008; 3:1101-1108.
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29. Marcotte M, Sharma R, Bouchard M. Gene regulatory network of renal primordium development. Pediatr Nephrol 2014; 29:637-644.
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30. Diav-Citrin O, Ornoy A. Selective serotonin reuptake inhibitors in human pregnancy: to treat or not to treat? Obstet Gynecol Int 2012; 2012:698947.
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31. Kallen BA, Otterblad Olausson P. Maternal use of selective serotonin re-uptake inhibitors in early pregnancy and infant congenital malformations. Birth Defects Res A Clin Mol Teratol 2007; 79:301-308.
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39. Daud AN, Bergman JE, Kerstjens-Frederikse WS, Groen H, Wilffert B. The risk of congenital heart anomalies following prenatal exposure to serotonin reuptake inhibitors-is pharmacogenetics the Key? Int J Mol Sci 2016; 17:1333.
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40. Kornum JB, Nielsen RB, Pedersen L, Mortensen PB, Norgaard M. Use of selective serotonin-reuptake inhibitors during early pregnancy and risk of congenital malformations: updated analysis. Clin Epidemiol 2010; 2:29-36.
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43
ORIGINAL_ARTICLE
Effects of salidroside on rat CYP enzymes by a cocktail of probe drugs
Objective(s): In this study, we aimed to evaluate the effect of salidroside on the activities of the different drug-metabolizing enzymes CYP1A2, CYP2B6, CYP2C9, CYP2D6 and CYP3A4 in rats, in which a specific probe drug was used for each enzyme. Materials and Methods: After pretreatment with salidroside, five probe drugs were simultaneously administered to rats by gavage. The given dose was 2.0 mg/kg for phenacetin (CYP1A2 activity), 4.0 mg/kg for bupropion (CYP2B6 activity), 2.0 mg/kg for losartan (CYP2C9 activity), 8.0 mg/kg for metoprolol (CYP2D6 activity) and 1.0 mg/kg for midazolam (CYP3A4 activity). Then, an ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was used to analyze the concentrations of rats’ blood, which were collected at different corresponding times. Results: Our data showed that salidroside exhibited an inductive effect on CYP1A2, CYP2B6, CYP2C9 and CYP3A4 activities by changing the main pharmacokinetic parameters (t1/2, CL/F, Cmax and AUC(0-∞)) of the four probe drugs in rats. However, no significant changes in CYP2D6 activity were observed. Conclusion: In a word, the results displayed that salidroside could induce the activities of CYP1A2, CYP2B6, CYP2C9 and CYP3A4, which may influence the disposition of the drugs that are mainly metabolized by these pathways. Our research can provide the basis for the study of related herb-drug interactions in clinic.
https://ijbms.mums.ac.ir/article_10464_29b14db2f2ecef81dcfcba9e153e2f2b.pdf
2018-04-01
422
426
10.22038/ijbms.2018.26106.6414
Cytochrome P450
Cocktail
Enzyme
Herb-drug interaction
Salidroside
Yan-Li
Wei
wei0579du@163.com
1
Jinhua Polytechnic, Jinhua 321007, Zhejiang, PR China
AUTHOR
Hong-Jian
Du
zjjhdhj@163.com
2
Jinhua Polytechnic, Jinhua 321007, Zhejiang, PR China
AUTHOR
Yi-Ping
Lin
2424514192@qq.com
3
Jinhua Polytechnic, Jinhua 321007, Zhejiang, PR China
AUTHOR
Mei-Ling
Wu
550997006@qq.com
4
Jinhua Polytechnic, Jinhua 321007, Zhejiang, PR China
AUTHOR
Ren-ai
Xu
xurenai1986@163.com
5
The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang, PR China
LEAD_AUTHOR
1. Zhou SF, Liu JP, and Chowbay B. Polymorphism of human cytochrome P450 enzymes and its clinical impact. Drug Metab Rev 2009; 41:89-295.
1
2. Wrighton SA, VandenBranden M, and Ring BJ. The human drug metabolizing cytochromes P450. J Pharmacokinet Biopharm 1996; 24:461-473.
2
3. Meyer UA. Overview of enzymes of drug metabolism. J Pharmacokinet Biopharm 1996; 24:449-459.
3
4. Breimer DD. Interindividual variations in drug disposition. Clinical implications and methods of investigation. Clin Pharmacokinet 1983; 8:371-377.
4
5. Zhou CJ, Qiao LM, Zhao LH, and Li ZY. Evaluation of the impact of cantharidin on rat CYP enzymes by using a cocktail of probe drugs. Fitoterapia 2015; 107:49-53.
5
6. Geng P, Wang S, Wang C, Chen J, Zhang L, Yang S, et al. Evaluation of the impact of Flos Daturae on rat hepatic cytochrome P450 enzymes by cocktail probe drugs. Int J Clin Exp Med 2015; 8:22310-8.
6
7. Wu Q, Zhang Q, Wen C, Hu L, Wang X, and Lin G. The effect of MS-275 on CYP450 isoforms activity in rats by cocktail method. Int J Clin Exp Pathol 2015; 8:9360-7.
7
8. Zhang YT, Zhang DF, Ge NY, Zhu GH, Hao C, Zhang Y, et al. effect of evodiamine on CYP enzymes in rats by a cocktail method. Pharmacology 2016; 97:218-223.
8
9. Xu RA, Xu ZS, and Ge RS. Effects of hydroxysafflor yellow A on the activity and mRNA expression of four CYP isozymes in rats. J Ethnopharmacol 2014; 151:1141-1146.
9
10. Huang Y, Zheng SL, Zhu HY, Xu ZS, and Xu RA. Effects of aescin on cytochrome P450 enzymes in rats. J Ethnopharmacol 2014; 151:583-590.
10
11. Hung SK, Perry R, and Ernst E. The effectiveness and efficacy of Rhodiola rosea L.: a systematic review of randomized clinical trials. Phytomedicine 2011; 18:235-244.
11
12. Spasov AA, Wikman GK, Mandrikov VB, Mironova IA, and Neumoin VV. A double-blind, placebo-controlled pilot study of the stimulating and adaptogenic effect of Rhodiola rosea SHR-5 extract on the fatigue of students caused by stress during an examination period with a repeated low-dose regimen. Phytomedicine 2000; 7:85-89.
12
13. Zhang H, Shen WS, Gao CH, Deng LC, and Shen D. Protective effects of salidroside on epirubicin-induced early left ventricular regional systolic dysfunction in patients with breast cancer. Drugs R D 2012; 12:101-106.
13
14. Shi TY, Feng SF, Xing JH, Wu YM, Li XQ, Zhang N, et al. Neuroprotective effects of salidroside and its analogue tyrosol galactoside against focal cerebral ischemia in vivo and H2O2-induced neurotoxicity in vitro. Neurotox Res 2012; 21:358-367.
14
15. Zhang JK, Yang L, Meng GL, Yuan Z, Fan J, Li D, et al. Protection by salidroside against bone loss via inhibition of oxidative stress and bone-resorbing mediators. PLoS One 2013; 8:e57251.
15
16. Li D, Fu Y, Zhang W, Su G, Liu B, Guo M, et al. Salidroside attenuates inflammatory responses by suppressing nuclear factor-kappaB and mitogen activated protein kinases activation in lipopolysaccharide-induced mastitis in mice. Inflamm Res 2013; 62:9-15.
16
17. Guan S, He J, Guo W, Wei J, Lu J, and Deng X. Adjuvant effects of salidroside from Rhodiola rosea L. on the immune responses to ovalbumin in mice. Immunopharmacol Immunotoxicol 2011; 33:738-743.
17
18. Zhao G, Shi A, Fan Z, and Du Y. Salidroside inhibits the growth of human breast cancer in vitro and in vivo. Oncol Rep 2015; 33:2553-2560.
18
19. Sun KX, Xia HW, and Xia RL. Anticancer effect of salidroside on colon cancer through inhibiting JAK2/STAT3 signaling pathway. Int J Clin Exp Pathol 2015; 8:615-621.
19
20. Wang J, Li JZ, Lu AX, Zhang KF, and Li BJ. Anticancer effect of salidroside on A549 lung cancer cells through inhibition of oxidative stress and phospho-p38 expression. Oncol Lett 2014; 7:1159-1164.
20
21. Wei YL, Du HJ, Lin YP, Wu ML, Ying XQ, Ding MX, et al. Simultaneous Determination of Five Rat CYP450 Probe Drugs by UPLC-MS/MS Method. Lat Am J Pharm 2016; 35:1810-1815.
21
22. Shimada T, Yamazaki H, Mimura M, Inui Y, and Guengerich FP. Interindividual variations in human liver cytochrome P-450 enzymes involved in the oxidation of drugs, carcinogens and toxic chemicals: studies with liver microsomes of 30 Japanese and 30 Caucasians. J Pharmacol Exp Ther 1994; 270:414-423.
22
23. Stresser DM and Kupfer D. Monospecific antipeptide antibody to cytochrome P-450 2B6. Drug Metab Dispos 1999; 27:517-525.
23
24. Miners JO and Birkett DJ. Cytochrome P4502C9: an enzyme of major importance in human drug metabolism. Br J Clin Pharmacol 1998; 45:525-538.
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25. Zhou SF. Polymorphism of human cytochrome P450 2D6 and its clinical significance: Part I. Clin Pharmacokinet 2009; 48:689-723.
25
26. Zhou SF. Polymorphism of human cytochrome P450 2D6 and its clinical significance: part II. Clin Pharmacokinet 2009; 48:761-804.
26
ORIGINAL_ARTICLE
Inhibition of breast cancer metastasis by co-transfection of miR-31/193b-mimics
Objective(s): Various studies have been conducted to reduce the metastatic behavior of cancerous cells. In this regard, ectopic expression of anti-metastatic microRNAs by miR-mimic and miR-restoration-based therapies could bring new insights to the field. In the present study, the consequences of co-transfecting breast cancer cell lines with miR-193b and miR-31 were investigated via invasion and migration assays.Materials and Methods: Double stranded oligonucleotide of mature miR-193b-3p and miR-31-5p were cloned into pcDNA 6.2gw/EmGFP plasmid. The resulting plasmids were used for transfection. Real time-PCR was performed to assess the expression of miR-193b and miR-31 as well as Ras homolog gene family member A (RhoA) and urokinase-type plasminogen activator (uPA) as miR targets. Scratch, Transwell migration and Matrigel invasion assays were carried out to assess the extent of migration and invasion of cell lines.Results: The most significant increase in expression of miRs belonged to the single transfection of mimic-miRs in MDA-MB231. Although the co-transfection was not as successful as single transfection in miR expression, it was significantly more effective in inhibition of the cells invasive potential. Conclusion: Although the miR-restoration therapy based on co-transfection of two miRs could be less effective in expression of each miRNA, the resulting decrease in metastatic behavior of the cells is more significant due to collective effect of co-transfection to decrease target gene expression. Our results revealed that employing this sort of combinatorial strategies could lead to more efficient reduction in metastatic behavior. It seems that using this strategy would bring about more successful therapeutic outcomes.
https://ijbms.mums.ac.ir/article_10465_66763c2c7b92b4a7a96834186ac01bb0.pdf
2018-04-01
427
433
10.22038/ijbms.2018.26614.6522
Breast Cancer
Metastasis
miR-31
miR-193b
RhoA
uPA
Zahra Sadat
Hashemi
z.hashemi87@gmail.com
1
Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
mehdi
Forouzandeh Moghadam
foroz@modares.ac.ir
2
Department of Medical Biotechnology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
AUTHOR
Samila
Farokhimanesh
s.farokhimanesh@modares.ac.ir
3
Department of Medical Biotechnology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
AUTHOR
masuomeh
rajabibazl
rajabibazl_m@yahoo.com
4
Department of Clinical Biochemistry, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Esmaeil
sadroddiny
sadroddiny@sina.tums.ac.ir
5
Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2016. CA Cancer J Clin 2016; 66:7-30.
1
2. Eccles SA, Welch DR. Metastasis: recent discoveries and novel treatment strategies. Lancet 2007; 369:1742-1757.
2
3. Hashemi ZS, Forouzandeh Moghadam M, Soleimani M. Comparison of TGFbR2 down-regulation in expanded HSCs on MBA/DBM scaffolds coated by UCB stromal cells. In Vitro Cell Dev Biol Anim 2015; 51:495-506.
3
4. Choghaei E, Khamisipour G, Falahati M, Naeimi B, Mossahebi-Mohammadi M, Tahmasebi R, et al. Knockdown of microRNA-29a Changes the Expression of Heat Shock Proteins in Breast Carcinoma MCF-7 Cells. Oncol Res 2016; 23:69-78.
4
5. Farokhimanesh S, Forouzandeh Moghadam M, Ebrahimi M, Ghamnak A, Hashemi ZS. Synthetic canonical miR-31, a pleiotropically acting anti-metastasis miR-based therapeutic in invasive breast cancer. Res Pharm Sci 2012; 7:S495.
5
6. Farokhimanesh S, Forouzandeh Moghadam M, Ebrahimi M, Hashemi ZS, Ghamnak A. Stemness inhibiting mir-200 family target sequence for translational repression of therapeutic gene in cancer stem cell rich MDA-MB231 cell line; POSTER PRESENTATION. Cell J 2012.
6
7. Hashemi ZS, Khalili S, Forouzandeh Moghadam M, Sadroddiny E. Lung cancer and miRNAs: a possible remedy for anti-metastatic, therapeutic and diagnostic applications. Expert Rev Respir Med 2017; 11:147-157.
7
8. Kouhkan F, Mohamadi Mosahebi M, Mohamadi S, Khamisipour G, Soufizomorrod M, Hashemi ZS, et al. Evaluation of microRNA-16 functions in breast cancer; POSTER PRESENTATION. Cell J 2012.
8
9. Langroudi L, Forouzandeh M, Soleimani M, Atashi A, Golestaneh AF. Induction of differentiation by down-regulation of Nanog and Rex-1 in cord blood derived unrestricted somatic stem cells. Mol Biol Rep 2013; 40:4429-4437.
9
10. Mohammadpour H, Khalili S, Hashemi ZS. Kremen is beyond a subsidiary co-receptor of Wnt signaling: an in silico validation. Turk J Biol 2015; 39:501-510.
10
11. Hashemi ZS, Forouzandeh Moghadam M, Soleimani M, Hafizi M, Amirizadeh N. TGF-b downregulation by RNAi technique in ex vivo-expanded HSCs on 3D DBM scaffold. Teh Univ Med Sci 2012; 70.
11
12. Khalili S, Rasaee M, Bamdad T. 3D structure of DKK1 indicates its involvement in both canonical and non-canonical Wnt pathways. Mol Biol (Mosk) 2017; 51:155-166.
12
13. Hashemi ZS, Forouzandeh Moghadam M, Soleimani M. Comparison of the ex vivo expansion of UCB-derived CD34+ in 3D DBM/MBA scaffolds with USSC as a feeder layer. Iran J Basic Med Sci 2013; 16:1075-1087.
13
14. Garofalo M, Croce CM. microRNAs: Master regulators as potential therapeutics in cancer. Annu Rev Pharmacol Toxicol 2011; 51:25-43.
14
15. Nassar FJ, Nasr R, Talhouk R. MicroRNAs as biomarkers for early breast cancer diagnosis, prognosis and therapy prediction. Pharmacol Ther 2016.
15
16. Banaei-Esfahani A, Moazzeni H, Nosar PN, Amin S, Arefian E, Soleimani M, et al. MicroRNAs that target RGS5. Iran J Basic Med Sci 2015; 18:108.
16
17. Hurst DR, Edmonds MD, Welch DR. Metastamir: the field of metastasis-regulatory microRNA is spreading. Cancer Res. 2009; 69:7495-7498.
17
18. Felekkis K, Touvana E, Stefanou C, Deltas C. microRNAs: a newly described class of encoded molecules that play a role in health and disease. Hippokratia 2010; 14:236.
18
19. Mitchell PS, Parkin RK, Kroh EM, Fritz BR, Wyman SK, Pogosova-Agadjanyan EL, et al. Circulating microRNAs as stable blood-based markers for cancer detection. Proc Natl Acad Sci U S A 2008; 105:10513-10518.
19
20. Ng EK, Li R, Shin VY, Jin HC, Leung CP, Ma ES, et al. Circulating microRNAs as specific biomarkers for breast cancer detection. PLoS One 2013; 8:e53141.
20
21. Lu Z, Ye Y, Jiao D, Qiao J, Cui S, Liu Z. miR-155 and miR-31 are differentially expressed in breast cancer patients and are correlated with the estrogen receptor and progesterone receptor status. Oncol Lett 2012; 4:1027-1032.
21
22. Valastyan S, Weinberg RA. miR-31: a crucial overseer of tumor metastasis and other emerging roles. Cell Cycle 2010; 9:2124-2129.
22
23. Valastyan S, Weinberg RA. Roles for microRNAs in the regulation of cell adhesion molecules. J Cell Sci 2011; 124:999-1006.
23
24. Chen J, Feilotter HE, Paré GC, Zhang X, Pemberton JG, Garady C, et al. MicroRNA-193b represses cell proliferation and regulates cyclin D1 in melanoma. Am J Pathol 2010; 176:2520-2529.
24
25. Hu H, Li S, Liu J, Ni B. MicroRNA-193b modulates proliferation, migration, and invasion of non-small cell lung cancer cells. Acta Biochim Biophys Sin (Shanghai) 2012; 44:424-340.
25
26. Zhong Q, Wang T, Lu P, Zhang R, Zou J, Yuan S. miR-193b promotes cell proliferation by targeting Smad3 in human glioma. J Neurosci Res 2014; 92:619-626.
26
27. Li X, Yan P, Shao Z. Downregulation of miR-193b contributes to enhance urokinase-type plasminogen activator (uPA) expression and tumor progression and invasion in human breast cancer. Oncogene 2009; 28:3937-3948.
27
28. Leivonen S, Mäkelä R, Östling P, Kohonen P, Haapa-Paananen S, Kleivi K, et al. Protein lysate microarray analysis to identify microRNAs regulating estrogen receptor signaling in breast cancer cell lines. Oncogene 2009; 28:3926-3936.
28
29. Gruppen F. MicroRNAs in breast cancer 2011.
29
30. Tang F, Zhang R, He Y, Zou M, Guo L, Xi T. MicroRNA-125b induces metastasis by targeting STARD13 in MCF-7 and MDA-MB-231 breast cancer cells. PLoS One 2012;7:e35435.
30
31. Rasheed SAK, Teo CR, Beillard EJ, Voorhoeve PM, Zhou W, Ghosh S, et al. MicroRNA-31 controls G protein alpha-13 (GNA13) expression and cell invasion in breast cancer cells. Mol Cancer 2015; 14:1.
31
32. Körner C, Keklikoglou I, Bender C, Wörner A, Münstermann E, Wiemann S. MicroRNA-31 Sensitizes Human Breast Cells to Apoptosis by Direct Targeting of Protein Kinase C ϵ (PKCϵ). J Biol Chem 2013; 288:8750-8761.
32
33. Long J, Ji Z, Jiang K, Wang Z, Meng G. miR-193b Modulates Resistance to Doxorubicin in Human Breast Cancer Cells by Downregulating MCL-1. Biomed Res Int 2015; 2015.
33
34. Hashemi ZS, Forouzandeh Moghadam M, Soleimani M. Comparison of TGFbR2 down-regulation in expanded HSCs on MBA/DBM scaffolds coated by UCB stromal cells. In Vitro Cell Dev Biol Anim 2015; 51:495-506.
34
35. Surks HK, Richards CT, Mendelsohn ME. Myosin Phosphatase-Rho Interacting Protein. A new member of the myosin phosphatase complex that directly binds RhoA. J Biol Chem 2003; 278:51484-51493.
35
36. Tang L, Han X. The urokinase plasminogen activator system in breast cancer invasion and metastasis. Biomed Pharmacother 2013; 67:179-182.
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37
ORIGINAL_ARTICLE
he effects of vitamin B12 on the brain damages caused by methamphetamine in mice
Objective(s): Methamphetamine (METH) is a powerful stimulant drug that directly affects the brain and induces neurological deficits. B12 is a water-soluble vitamin (vit) that is reported to attenuate neuronal degeneration. The goal of the present study is to investigate the effect of vitamin B12 on METH’s neurodegenerative changes.Materials and Methods: Two groups of 6 animals received METH (10 mg/kg, interaperitoneally (IP)) four times with a 2 hr interval. Thirty mins before METH administration, vit B12 (1 mg/kg) or normal saline were injected IP. Animals were sacrificed 3 days after the last administration. Caspase proteins levels were measured by Western blotting. Also, samples were examined by TUNEL assay to detect the presence of DNA fragmentation. Reduced glutathione (GSH) was also determined by the Ellman method.Results: The pathological findings showed that vit B12 attenuates the gliosis induced by METH. Vit B12 administration also significantly decreased the apoptotic index in the striatum and the cerebral cortex (P<0.001). It also reduced caspase markers compared to the control (PConclusion: The current study suggests that parenteral vit B12 at safe doses may be a promising treatment for METH-induced brain damage via inhibition of neuron apoptosis and increasing the reduced GSH level. Research focusing on the mechanisms involved in the protective responses of vit B12 can be helpful in providing a novel therapeutic agent against METH-induced neurotoxicity.
https://ijbms.mums.ac.ir/article_10466_e744fab65c3b61d699088d693dae0921.pdf
2018-04-01
434
438
10.22038/ijbms.2018.23362.5897
Cerebral cortex Methamphetamine Neurotoxicity
Striatum
Vitamin B12
Mohamad
Moshiri
moshirim@mums.ac.ir
1
Medical Toxicology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Seyed Mojtaba
Hosseiniyan
mojtaba.hoseinian68@gmail.com
2
Department of Toxicology, Faculty of Pharmacy, Islamic Azad University, Shahreza Branch, Shahreza, Iran
AUTHOR
Seyed Adel
Moallem
moallem@mums.ac.ir
3
Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Farzin
Hadizadeh
hadizadehf@mums.ac.ir
4
Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Amir Hosein
Jafarian
jafarianah@mums.ac.ir
5
Cancer Molecular Pathology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Ameneh
Ghadiri
ghadiria64@gmail.com
6
Department of Toxicology, Faculty of Pharmacy, Islamic Azad University, Shahreza Branch, Shahreza, Iran
AUTHOR
Toktam
Hoseini
hoseinit1@mums.ac.ir
7
Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mahmoud
Seifi
seifim1@mums.ac.ir
8
Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
leila
etemad
etemadl@mums.ac.ir
9
Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
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