ORIGINAL_ARTICLE
The genus Cuscuta (Convolvolaceac): An updated review on indigenous uses, phytochemistry, and pharmacology
Cuscuta, commonly known as dodder, is a genus of family convolvolaceace. Approximately 170 species of Cuscuta are extensively distributed in temperate and subtropical areas of the world. Species of this genus are widely used as essential constituents in functional foods and traditional medicinal systems. Various parts of many members of Cuscuta have been found efficacious against a variety of diseases. Phytochemical investigations have confirmed presence of biologically active moieties such as flavonoids, alkaloids, lignans, saponines, phenolics, tannins, and fatty acids. Pharmacological studies and traditional uses of these plants have proved that they are effective antibacterial, antioxidant, antiostioporotic, hepatoprotective, anti-inflammatory, antitumor, antipyretic, antihypertensive, analgesic, anti hair fall, and antisteriogenic agents.
https://ijbms.mums.ac.ir/article_13964_508941f077531179def14caa6fc447aa.pdf
2019-11-01
1225
1252
10.22038/ijbms.2019.35296.8407
Bioactive
Cuscuta
Folk medicines
Pharmacological activities
Phytochemicals
Shazia
Noureen
shazianoureen11@gmail.com
1
Department of Chemistry, University of Sargodha, Sargodha-40100, Pakistan
AUTHOR
Sobia
Noreen
sobianoreen@uos.edu.pk
2
Department of Chemistry, University of Sargodha, Sargodha-40100, Pakistan
LEAD_AUTHOR
Shazia Akram
Ghumman
shaziaghuman33@gmail.com
3
College of Pharmacy, University of Sargodha, Sargodha-40100, Pakistan
AUTHOR
Fozia
Batool
fozia.batool@uos.edu.pk
4
Department of Chemistry, University of Sargodha, Sargodha-40100, Pakistan
AUTHOR
Syed Nasir Abbas
Bukhari
snab_hussaini@yahoo.com
5
Department of Pharmaceutical Chemistry, College of Pharmacy, Jouf University, Aljouf, Sakaka2014, Saudi Arabia
AUTHOR
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327
ORIGINAL_ARTICLE
Conditioned medium obtained from human amniotic membrane-derived mesenchymal stem cell attenuates heart failure injury in rats
Objective(s): Heart failure (HF) is one of the leading causes of death worldwide. Due to beneficial effects of stem cells, paracrine secretion of them has recently been used by researchers. The purpose of this study was to investigate the effects of intravenous injection (IV) of conditioned medium (CM) of human amniotic membrane-derived mesenchymal stem cell (MSC-CM) on HF.Materials and Methods: Male Wistar rats (n=35, 180 g) were randomly divided into five groups: sham, HF, HF+MSC-CM, HF+culture medium and HF+phosphate-buffered saline (PBS). To induce HF, isoproterenol (170 mg/kg/d) was injected subcutaneously for 4 consecutive days. After 28 days, induction of HF was evaluated by echocardiography. A day after echocardiography, 50 μg culture medium/5 ml PBS in HF+culture medium group, 50 μg MSC-CM/5 ml PBS in HF+MSC-CM group and 5 ml PBS in HF+PBS group were injected two times for 4 successive days. The echocardiography was performed 4 weeks after the last injection of isoproterenol. To evaluate the fibrosis, morphology, and cardiac function, Trichrome Masson’s staining, Hematoxylin and Eosin staining and echocardiography were performed, respectively.Results: CM significantly increased fractional shortening and ejection fraction, and also significantly decreased apoptotic nuclear condensation. Moreover, significant decreased level of fibrosis and increased level of angiogenesis was observed in the treatment group (P<0.05).Conclusion: Our results indicated that IV injection of CM has therapeutic effects on HF by reducing fibrosis and preventing the progression of failure due to its paracrine effects.
https://ijbms.mums.ac.ir/article_13723_0c2deee01cb4a45c1224669945a1fa78.pdf
2019-11-01
1253
1258
10.22038/ijbms.2019.36617.8722
Adipose tissue-derived-mesenchymal stem cells
Apoptosis
Conditioned medium
Fibrosis
heart failure
Solmaz
Nasseri Maleki
snms1369@gmail.com
1
Physiology Research Center and Department of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
Nahid
Aboutaleb
dr_nabo40@yahoo.com
2
Physiology Research Center and Department of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Donya
Nazarinia
e_nazarinia@yahoo.com
3
Department of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
Sara
Allahverdi Beik
sara.allahverdi@gmail.com
4
Physiology Research Center and Department of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
Asadollah
Qolamian
gh.biology@gmail.com
5
Physiology Research Center and Department of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
Maliheh
Nobakht
nobakhat@yahoo.com
6
Department of Histology and Neuroscience, Anti-microbial Resistance Research Center, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
1. Cowie M, Wood D, Coats A, Thompson S, Suresh V, Poole-Wilson P, et al. Survival of patients with a new diagnosis of heart failure: a population based study. Heart 2000; 83:505-510.
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4. Amani H, Habibey R, Hajmiresmail S, Latifi S, Pazoki-Toroudi H, Akhavan O. Antioxidant nanomaterials in advanced diagnoses and treatments of ischemia reperfusion injuries. J Mater Chem B 2017; 5:9452-9476.
4
5. Amani H, Ajami M, Maleki SN, Pazoki-Toroudi H, Daglia M, Sokeng AJT, et al. Targeting signal transducers and activators of transcription (STAT) in human cancer by dietary polyphenolic antioxidants. Biochimie 2017; 142:63-79.
5
6. Ajami M, Davoodi SH, Habibey R, Namazi N, Soleimani M, Pazoki‐Toroudi H, et al. Effect of DHA+ EPA on oxidative stress and apoptosis induced by ischemia‐reperfusion in rat kidneys. Fundam Clin Pharmacol 2013; 27:593-602.
6
7. Habibey R, Ajami M, Ebrahimi SA, Hesami A, Babakoohi S, Pazoki-Toroudi H, et al. Nitric oxide and renal protection in morphine-dependent rats. Free Radic Biol Med 2010; 49:1109-1118.
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8. Passier R, van Laake LW, Mummery CL. Stem-cell-based therapy and lessons from the heart. Nature 2008; 453:322-329.
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9. Amani H, Mostafavi E, Arzaghi H, Davaran S, Akbarzadeh A, Akhavan O, et al. Three-Dimensional Graphene Foams: Synthesis, Properties, Biocompatibility, Biodegradability, and Applications in Tissue Engineering. ACS Biomater Sci Eng 2019; 5:193-214.
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10. Teerlink JR, Metra M, Filippatos GS, Davison BA, Bartunek J, Terzic A, et al. Benefit of cardiopoietic mesenchymal stem cell therapy on left ventricular remodelling: results from the Congestive Heart Failure Cardiopoietic Regenerative Therapy (CHART‐1) study. Eur J Heart Fail 2017; 19:1520-1529.
10
11. Bartolucci J, Verdugo FJ, González PL, Larrea RE, Abarzua E, Goset C, et al. Safety and efficacy of the intravenous infusion of umbilical cord mesenchymal stem cells in patients with heart failure: a phase 1/2 randomized controlled trial (RIMECARD trial [randomized clinical trial of intravenous infusion umbilical cord mesenchymal stem cells on cardiopathy]). Circ Res 2017; 121:1192-1204.
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12. Halkos ME, Zhao Z-Q, Kerendi F, Wang N-P, Jiang R, Schmarkey LS, et al. Intravenous infusion of mesenchymal stem cells enhances regional perfusion and improves ventricular function in a porcine model of myocardial infarction. Basic Res Cardiol 2008; 103:525-536.
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13. Patel AN, Silva F, Winters AA. Stem cell therapy for heart failure. Heart Fail Clin. 2015; 11:275-286.
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14. Tse HF, Siu CW, Zhu SG, Songyan L, Zhang QY, Lai WH, et al. Paracrine effects of direct intramyocardial implantation of bone marrow derived cells to enhance neovascularization in chronic ischaemic myocardium. Eur J Heart Fail 2007; 9:747-753.
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15. Vulliet PR, Greeley M, Halloran SM, MacDonald KA, Kittleson MD. Intra-coronary arterial injection of mesenchymal stromal cells and microinfarction in dogs. Lancet 2004; 363:783-784.
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16. Trounson A, McDonald C. Stem cell therapies in clinical trials: progress and challenges. Cell Stem Cell 2015; 17:11-22.
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17. Gnecchi MJSctm. Cell therapy for heart regeneration: Learning from the past to build a brighter future. Stem Cells Translational Medicine 2018;7:702–704.
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18. Arsalan M, Dhein S, Aupperle H, Rastan AJ, Barten MJ, Walther T, et al. The reverse remodeling effect of mesenchymal stem cells is independent from the site of epimyocardial cell transplantation. Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery. Innovations (Phila) 2013; 8:433-439.
18
19. Bing W, Pang X, Qu Q, Bai X, Yang W, Bi Y, et al. Simvastatin improves the homing of BMSC s via the PI 3K/AKT/miR‐9 pathway. J Cell Mol Med 2016; 20:949-961.
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20. Baglio SR, Pegtel DM, Baldini N. Mesenchymal stem cell secreted vesicles provide novel opportunities in (stem) cell-free therapy. Front Physiol 2012; 3:359.
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21. Gnecchi M, Danieli P, Malpasso G, Ciuffreda MC. Paracrine mechanisms of mesenchymal stem cells in tissue repair. Methods Mol Biol 2016; 1416:123-146.
21
22. Aboutaleb N, Faezi M, Maleki SN, Nazarinia D, Tousi SMTR, Hashemirad NJJoCN. Conditioned medium obtained from mesenchymal stem cells attenuates focal cerebral ischemia reperfusion injury through activation of ERK1/ERK2-BDNF signaling pathway. J Chem Neuroanat 2019; 97:87-98.
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23. Cunningham CJ, Redondo-Castro E, Allan SMJJoCBF, Metabolism. The therapeutic potential of the mesenchymal stem cell secretome in ischaemic stroke. J Cereb Blood Flow Metab 2018; 38:1276-1292.
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24. Rehman J, Traktuev D, Li J, Merfeld-Clauss S, Temm-Grove CJ, Bovenkerk JE, et al. Secretion of angiogenic and antiapoptotic factors by human adipose stromal cells. Circulation 2004; 109:1292-1298.
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25. Barile L, Biemmi V, Ciullo A, Torre T, Demerzis S, Mauri P, et al. P4224 Superior exosome-mediated paracrine effects of cardiac progenitor cells compared to bone marrow mesenchymal stem cells derived from the same patient for cardiac repair. Eur Heart J 2018; 39:ehy563.P4224.
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26. Kervadec A, Bellamy V, El Harane N, Arakélian L, Vanneaux V, Cacciapuoti I, et al. Cardiovascular progenitor–derived extracellular vesicles recapitulate the beneficial effects of their parent cells in the treatment of chronic heart failure. J Heart Lung Transplant 2016; 35:795-807.
26
27. Golle L, Gerth HU, Beul K, Heitplatz B, Barth P, Fobker M, et al. Bone marrow-derived cells and their conditioned medium induce microvascular repair in uremic rats by stimulation of endogenous repair mechanisms. Sci Rep 2017;7:9444.
27
28. Faezi M, Maleki SN, Aboutaleb N, Nikougoftar. The membrane mesenchymal stem cell derived conditioned medium exerts neuroprotection against focal cerebral ischemia by targeting apoptosis. J Chem Neuroanat 2018; 94:21-31.
28
29. Liu Y-H, Lu M, Xie Z-Z, Hua F, Xie L, Gao JH, et al. Hydrogen sulfide prevents heart failure development via inhibition of renin release from mast cells in isoproterenol-treated rats. Antioxid Redox Signal 2014; 20:759-769.
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30. Pazoki-Toroudi H, Amani H, Ajami M, Nabavi SF, Braidy N, Kasi PD, et al. Targeting mTOR signaling by polyphenols: a new therapeutic target for ageing. Ageing Res Rev 2016; 31:55-66.
30
31. Mehrjerdi FZ, Aboutaleb N, Pazoki-Toroudi H, Soleimani M, Ajami M, Khaksari M, et al. The protective effect of remote renal preconditioning against hippocampal ischemia reperfusion injury: role of KATP channels. J Mol Neurosci 2015; 57:554-560.
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32. Pazoki‐Toroudi HR, Ajami M, Habibey R. Pre‐medication and renal pre‐conditioning: a role for alprazolam, atropine, morphine and promethazine. Fundamental Clin Pharmacol 2010; 24:189-198.
32
33. Habibey R, Pazoki‐Toroudi HJC, Pharmacology E, Physiology. Morphine dependence protects rat kidney against ischaemia–reperfusion injury. Clin Exp Pharmacol Physiol 2008; 35:1209-1214.
33
34. Ajami M, Pazoki-Toroudi H, Amani H, Nabavi SF, Braidy N, Vacca RA, et al. Therapeutic role of sirtuins in neurodegenerative disease and their modulation by polyphenols. Neurosci Biobehav Rev, 2017; 73:39-47.
34
35. Höglund M. Stem cell transplantation. HemaSphere 2018; 2:159.
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36. Naderi‐Meshkin H, Bahrami AR, Bidkhori HR, Mirahmadi M, Ahmadiankia N. Strategies to improve homing of mesenchymal stem cells for greater efficacy in stem cell therapy. Cell Biol Int 2015; 39:23-34
36
37. Luger D, Lipinski MJ, Westman PC, Glover DK, Frias JC, Albelda M, et al. Intravenously-delivered mesenchymal stem cells: systemic anti-inflammatory effects improve left ventricular dysfunction in acute myocardial infarction and ischemic cardiomyopathy. Circ Res 2017; 120:1598-1613.
37
38. Kim W-S, Park B-S, Sung J-H. The wound-healing and antioxidant effects of adipose-derived stem cells. Expert Opin Biol Ther 2009; 9:879-887.
38
39. Wang CY, Yang HB, Hsu HS, Chen LL, Tsai CC, Tsai KS, et al. Mesenchymal stem cell‐conditioned medium facilitates angiogenesis and fracture healing in diabetic rats. J Tissue Eng Regen Med 2012; 7:559-569.
39
40. Li Z, Guo J, Chang Q, Zhang A. Paracrine role for mesenchymal stem cells in acute myocardial infarction. Biol Pharm Bull 2009; 32:1343-1346.
40
41.Timmers L, Lim SK, Hoefer IE, Arslan F, Lai RC, van Oorschot AA, et al. Human mesenchymal stem cell-conditioned medium improves cardiac function following myocardial infarction. Stem Cell Res. (Amst.), 2011; 6:206-214.
41
ORIGINAL_ARTICLE
Thalidomide attenuates the hyporesponsiveness of isolated atria to chronotropic stimulation in BDL rats: The involvement of TNF-α, IL-6 inhibition, and SOCS1 activation
Objective(s): Cirrhotic cardiomyopathy is a complication of uncured cirrhosis which is associated with hyporesponsiveness of the heart to sympathetic stimulation. The enhancement of portal pressure, nitric oxide (NO) level, pro-inflammatory mediators and down-regulation of Suppressor of Cytokine Signaling 1 (SOCS1) are involved in this situations. The present study seeks to examine the beneficial effect of thalidomide on cirrhotic cardiomyopathy. Materials and Methods: The male rats were grouped as: Sham/saline, Sham/Thalidomide, Bile Duct Ligation (BDL)/saline and BDL/Thalidomide. BDL model of cirrhosis was used. In the treatment groups, thalidomide (200 mg/kg/day) was administrated by intragastrial gavage for 28 consecutive days, the chronotropic response was assessed in isolated atria by isoproterenol stimulation. Serum levels of NO, IL-6 and TNF-α hepatic level were evaluated. The intrasplenic pulp pressure (ISPP) as the portal pressure and histopathologic assessment were assessed. Real time RT-PCR was used for the evaluation of SOCS1 gene expression.Results: Our results showed that thalidomide administration could significantly increase the atrial chronotropic response in BDL animals. The increased level of portal pressure decreased by thalidomide in BDL animals. Thalidomide could ameliorate the histopathological conditions of BDL rats. Furthermore, the chronic treatment by this drug diminished the elevated levels of NO, TNF-α and IL-6 in BDL animals. On the other hand, hepatic SOCS1 expression was up-regulated by thalidomide treatment in this group. Conclusion: Thalidomide improves the chronotropic hyporesponsiveness of isolated atria in BDL. This effect is probably mediated by the inhibiting NO, TNF-α and IL-6 production, reducing portal pressure and increasing the expression of SOCS1.
https://ijbms.mums.ac.ir/article_13886_0783b44401da8d35992d9e5ddb361bea.pdf
2019-11-01
1259
1266
10.22038/ijbms.2019.32256.7742
Cirrhotic cardiomyopathy
IL-6
SOCS1
Thalidomide
TNF-α
Ali
Hosseini-chegeni
hosseiniheshmat@gmail.com
1
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
farahnaz
Jazaeri
fjazaeri@yahoo.com
2
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Aliakbar
Yousefi-Ahmadipour
lab.aliakbar@yahoo.com
3
Department of Laboratory of Sciences, Faculty of Paramedical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
AUTHOR
Mansour
Heidari
mheidari@sina.tums.ac.ir
4
Department of Medical Genetics, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Alireza
Abdollahi
dr_p_abdollahi@yahoo.com
5
Department of Pathology, School of Medicine, Imam Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Ahmad Reza
Dehpour
dehpour@yahoo.com
6
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1. Fernandez-Martinez E, Perez-Alvarez V, Tsutsumi V, Shibayama M, Muriel P. Chronic bile duct obstruction induces changes in plasma and hepatic levels of cytokines and nitric oxide in the rat. Exp Toxicol Pathol 2006;58:49-58.
1
2. Bernardi M. Cirrhotic cardiomyopathy. Clin Liver Dis 2013;2:99-101.
2
3. Møller S, Henriksen J H. Cirrhotic cardiomyopathy. J Hepatol 2010;53:179-190.
3
4. Choi I, Kang H S, Yang Y, Pyun K H. IL-6 induces hepatic inflammation and collagen synthesis in vivo. Clin Exp Immunol 1994;95:530-535.
4
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25. Das S, Santra A, Lahiri S, Mazumder D G. Implications of oxidative stress and hepatic cytokine (TNF-α and IL-6) response in the pathogenesis of hepatic collagenesis in chronic arsenic toxicity. Toxicol Appl Pharmacol 2005;204:18-26.
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35. Jazaeri F, Tavangar S M, Ghazi‐Khansari M, Khorramizadeh M R, Mani A R, Dehpour A R. Cirrhosis is associated with development of tolerance to cardiac chronotropic effect of endotoxin in rats. Liver Int 2013;33:368-374.
35
ORIGINAL_ARTICLE
The prevalence of exotoxins, adhesion, and biofilm-related genes in Staphylococcus aureus isolates from the main burn center of Tehran, Iran
Objective(s): The present study investigated the prevalence of genes encoding for exotoxins, adhesion and biofilm factors in Staphylococcus aureus isolates obtained from samples in a referral burn hospital in Tehran, Iran.Materials and Methods: S. aureus isolates obtained from patients, personnel and surfaces in the wards of a burn hospital were identified and confirmed by biochemical and molecular tests, respectively. The susceptibility of isolates was determined using the disk diffusion method. Virulence factors were detected by multiplex PCR.Results: The frequency of hla, hlb, hld, hlg, tst and pvl genes was 92.8%, 34.7%, 89.8%, 11.9%, 10.7%, and 0.5% respectively. The results revealed that the hla gene had the highest frequency among isolates (94.4% for methicillin-resistant S. aureus (MRSA) and 89.8% for methicillin-susceptible S. aureus (MSSA)). The most prevalent adhesion and biofilm-related gene was eno (85.6%). The prevalence of the remaining genes was as follows: fib (71.8%), clfB (70%), cna (59.2 %), fnbB (17.9%), icaA (72.4%), and icaD (85.6%). The incidence of fib, hlb, hlg, and tst genes was significantly higher in MRSA isolates compare to the MSSA isolates. Moreover, the resistance rates for all antibiotics were higher is MRSA isolates except for nitrofurantoin and chloramphenicol antibiotics.Conclusion: Data indicate the high prevalence rates of virulence factors among S. aureus isolates, especially MRSA strains in the burn hospital. This should to be taken into account in the development of an effective infection control policy and continuous monitoring of drug resistance in hospitals.
https://ijbms.mums.ac.ir/article_13931_9b268d06e0f0510e28681b1e9dcffe6c.pdf
2019-11-01
1267
1274
10.22038/ijbms.2019.34908.8291
MRSA
virulence factors
Adhesin and biofilm genes
Burn
Iran
Zahra
Mir
mir500@gmail.com
1
Microbial Biotechnology Research Center, Department of Microbiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
Narges
Nodeh Farahani
farahani500@gmail.com
2
Microbial Biotechnology Research Center, Department of Microbiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
Sara
Abbasian
abbasian500@gmail.com
3
Microbial Biotechnology Research Center, Department of Microbiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
Faranak
Alinejad
alinejad500@gmail.com
4
Burn Research Center, Shahid Motahari Hospital, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
Mahboubeh
Sattarzadeh
sattarzadeh500@gmail.com
5
Burn Research Center, Shahid Motahari Hospital, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
Ramin
Pouriran
pouriran500@gmail.com
6
School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Mostafa
Dahmardehei
dahmardehei500@gmail.com
7
Burn Research Center, Shahid Motahari Hospital, Iran University of Medical Sciences, Tehran, Iran
AUTHOR
Mehdi
Mirzaii
mirzaii500@gmail.com
8
School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran
AUTHOR
Seyed Sajjad
Khoramrooz
khoramrooz500@gmail.com
9
Cellular and Molecular Research Center, Yasuj University of Medical Sciences, Yasuj, Iran
AUTHOR
Davood
Darban-Sarokhalil
davood_darban@yahoo.com
10
Microbial Biotechnology Research Center, Department of Microbiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1. Boers SA, van Ess I, Euser SM, Jansen R, Tempelman FR, Diederen BM. An outbreak of a multiresistant methicillin-susceptible Staphylococcus aureus (MR-MSSA) strain in a burn centre: the importance of routine molecular typing. Burns: Burns 2011;37:808-813.
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2
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3
4. Otto M. Staphylococcus aureus toxins. Curr Opin Microbiol 2014;17:32-37.
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7. Tristan A, Ying L, Bes M, Etienne J, Vandenesch F, Lina G. Use of multiplex PCR to identify Staphylococcus aureus adhesins involved in human hematogenous infections. J Clin Microbiol 2003;41:4465-4467.
7
8. den Reijer PM, Haisma EM, Lemmens-den Toom NA, Willemse J, Koning RI, Demmers JA, et al. Detection of alpha-toxin and other virulence factors in biofilms of Staphylococcus aureus on polystyrene and a human epidermal model. PLoS One 2016;11:e0145722.
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9. Archer NK, Mazaitis MJ, Costerton JW, Leid JG, Powers ME, Shirtliff ME. Staphylococcus aureus biofilms: properties, regulation, and roles in human disease. Virulence 2011;2:445-459.
9
10. Rodrigues MVP, Fortaleza CMCB, Riboli DFM, Rocha RS, Rocha C, de Souza MdLR. Molecular epidemiology of methicillin-resistant Staphylococcus aureus in a burn unit from Brazil. Burns 2013;39:1242-1249.
10
11. Darban-Sarokhalil D, Khoramrooz SS, Marashifard M, Hosseini SAAM, Parhizgari N, Yazdanpanah M, et al. Molecular characterization of Staphylococcus aureus isolates from southwest of Iran using spa and SCCmec typing methods. Microb Pathog 2016;98:88-92.
11
12. Bar-Gal GK, Blum SE, Hadas L, Ehricht R, Monecke S, Leitner G. Host-specificity of Staphylococcus aureus causing intramammary infections in dairy animals assessed by genotyping and virulence genes. Vet Microbiol 2015;176:143-154.
12
13. Japoni A, Jamalidoust M, Farshad S, Ziyaeyan M, Alborzi A, Japoni S, et al. Characterization of SCCmec types and antibacterial susceptibility patterns of methicillin-resistant Staphylococcus aureus in Southern Iran. Jpn J Infect Dis 2011;64:28-33.
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14. Vasudevan P, Nair MKM, Annamalai T, Venkitanarayanan KS. Phenotypic and genotypic characterization of bovine mastitis isolates of Staphylococcus aureus for biofilm formation. Vet Microbiol 2003;92:179-185.
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15. Jarraud S, Mougel C, Thioulouse J, Lina G, Meugnier H, Forey F, et al. Relationships between Staphylococcus aureus genetic background, virulence factors, agr groups (alleles), and human disease. Infect Immun 2002;70:631-641.
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16. Mehrotra M, Wang G, Johnson WM. Multiplex PCR for detection of genes forStaphylococcus aureus enterotoxins, exfoliative toxins, toxic shock syndrome toxin 1, and methicillin resistance. J Clin Microbiol 2000;38:1032-1035.
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17. Abbasi-Montazeri E, Khosravi AD, Feizabadi MM, Goodarzi H, Khoramrooz SS, Mirzaii M, et al. The prevalence of methicillin resistant Staphylococcus aureus (MRSA) isolates with high-level mupirocin resistance from patients and personnel in a burn center. Burns 2013;39:650-654.
17
18. Dibah S, Arzanlou M, Jannati E, Shapouri R. Prevalence and antimicrobial resistance pattern of methicillin resistant Staphylococcus aureus (MRSA) strains isolated from clinical specimens in Ardabil, Iran. Iran J Microbiol. 2014;6:163.
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19. Kooistra-Smid M, van Dijk S, Beerthuizen G, Vogels W, van Zwet T, van Belkum A, et al. Molecular epidemiology of Staphylococcus aureus colonization in a burn center. Burns 2004;30:27-33.
19
20. Parhizgari N, Khoramrooz SS, Hosseini M, Asghar SA, Marashifard M, Yazdanpanah M, et al. High frequency of multidrug‐resistant Staphylococcus aureus with SCCmec type III and Spa types t037 and t631 isolated from burn patients in Southwest of Iran. APMIS 2016;124:221-228.
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21. Kateete DP, Namazzi S, Okee M, Okeng A, Baluku H, Musisi NL, et al. High prevalence of methicillin resistant Staphylococcus aureus in the surgical units of Mulago hospital in Kampala, Uganda. BMC Res Notes 2011;4:326-330.
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22. Song W, Lee KM, Kang HJ, Shin DH, Kim DK. Microbiologic aspects of predominant bacteria isolated from the burn patients in Korea. Burns 2001;27:136-139.
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23. Alebachew T, Yismaw G, Derabe A, Sisay Z. Staphylococcus aureus burn wound infection among patients attending yekatit 12 hospital burn unit, addis ababa, ethiopia. Ethiop J Health Sci 2012;22:209-213.
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24. Khoramrooz SS, Dolatabad SA, Dolatabad FM, Marashifard M, Mirzaii M, Dabiri H, et al. Detection of tetracycline resistance genes, aminoglycoside modifying enzymes, and coagulase gene typing of clinical isolates of Staphylococcus aureus in the Southwest of Iran. Iran J Basic Med Sci 2017;20:912-919.
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25. Davies J, Davies D. Origins and evolution of antibiotic resistance. Microbiol Mol Biol Rev 2010;74:417-433.
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26. Bayat B, Zade MH, Mansouri S, Kalantar E, Kabir K, Zahmatkesh E, et al. High frequency of methicillin-resistant Staphylococcus aureus (MRSA) with SCCmec type III and spa type t030 in Karaj’s teaching hospitals, Iran. Acta Microbiol Immunol Hung 2017;64:331-341.
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27. Hetem DJ, Bonten MJ. Clinical relevance of mupirocin resistance in Staphylococcus aureus. J Hosp Infect 2013;85:249-256.
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28. Patel JB, Gorwitz RJ, Jernigan JA. Mupirocin resistance. Clin Infect Dis. 2009;49:935-941.
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29. Khoramrooz SS, Mansouri F, Marashifard M, Hosseini SAAM, Chenarestane-Olia FA, Ganavehei B, et al. Detection of biofilm related genes, classical enterotoxin genes and agr typing among Staphylococcus aureus isolated from bovine with subclinical mastitis in southwest of Iran. Microb Pathog 2016;97:45-51.
29
30. Motallebi M, Jabalameli F, Asadollahi K, Taherikalani M, Emaneini M. Spreading of genes encoding enterotoxins, haemolysins, adhesin and biofilm among methicillin resistant Staphylococcus aureus strains with staphylococcal cassette chromosome mec type IIIA isolated from burn patients. Microb Pathog 2016;97:34-37.
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31. Satorres SE, Alcaraz LE. Prevalence of icaA and icaD genes in Staphylococcus aureus and Staphylococcus epidermidis strains isolated from patients and hospital staff. Cent Eur J Public Health 2007;15:87-90.
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32. Haveri M, Hovinen M, Roslof A, Pyorala S. Molecular types and genetic profiles of Staphylococcus aureus strains isolated from bovine intramammary infections and extramammary sites. J Clin Microbiol 2008;46:3728-3735.
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33. Gharsa H, Dziri R, Klibi N, Chairat S, Lozano C, Torres C, et al. Environmental Staphylococcus aureus contamination in a Tunisian hospital. J Chemother 2016;28:506-509.
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34. Karmakar A, Dua P, Ghosh C. Biochemical and molecular analysis of Staphylococcus aureus clinical isolates from hospitalized patients. Can J Infect Dis Med Microbiol 2016;2016:9041636.
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35. Liu C, Chen ZJ, Sun Z, Feng X, Zou M, Cao W, et al. Molecular characteristics and virulence factors in methicillin-susceptible, resistant, and heterogeneous vancomycin-intermediate Staphylococcus aureus from central-southern China. J Microbiol Immunol Infec 2015;48:490-496.
35
36. Emaneini M, Khoramrooz SS, Shahsavan S, Dabiri H, Jabalameli F. Prevalence of Panton-Valentine leucocidin and phenotypic and genotypic characterization of biofilm formation among Staphylococcus aureus strains isolated from children with adenoid hypertrophy. Microb Pathog 2015;89:150-153.
36
37. Mkrtchyan HV, Xu Z, Yacoub M, Ter-Stepanyan MM, Karapetyan HD, Kearns AM, et al. Detection of diverse genotypes of methicillin-resistant Staphylococcus aureus from hospital personnel and the environment in Armenia. Antimicrob Resist Infect Control 2017;6:19-23.
37
38. Murray CK, Holmes RL, Ellis MW, Mende K, Wolf SE, McDougal LK, et al. Twenty-five year epidemiology of invasive methicillin-resistant Staphylococcus aureus (MRSA) isolates recovered at a burn center. Burns 2009;35:1112-1127.
38
39. Becker K, Roth R, Peters G. Rapid and specific detection of toxigenic Staphylococcus aureus: use of two multiplex PCR enzyme immunoassays for amplification and hybridization of staphylococcal enterotoxin genes, exfoliative toxin genes, and toxic shock syndrome toxin 1 gene. J Clin Microbiol 1998;36:2548-2553.
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41. Peck KR, Baek JY, Song JH, Ko KS. Comparison of genotypes and enterotoxin genes between Staphylococcus aureus isolates from blood and nasal colonizers in a Korean hospital. J Korean Med Sci 2009;24:585-591.
41
42. De Boeck H, Vandendriessche S, Hallin M, Batoko B, Alworonga JP, Mapendo B, et al. Staphylococcus aureus nasal carriage among healthcare workers in Kisangani, the Democratic Republic of the Congo. Eur J Clin Microbiol Infect Dis 2015;34:1567-1572.
42
43. Jaspers M, Breederveld R, Tuinebreijer W, Diederen B. The evaluation of nasal mupirocin to prevent Staphylococcus aureus burn wound colonization in routine clinical practice. Burns 2014;40:1570-1574.
43
44. Asadollahi P, Farahani NN, Mirzaii M, Khoramrooz SS, Van Belkum A, Asadollahi K, et al. Distribution of the most prevalent spa types among clinical isolates of methicillin-resistant and-susceptible Staphylococcus aureus around the world: A review. Front Microbiol 2018;9:163-178.
44
ORIGINAL_ARTICLE
Akt inhibitor deguelin aggravates inflammation and fibrosis in myocarditis
Objective(s): Myocarditis is characterized by inflammatory cell infiltration in myocardial stroma. Attenuation of tumor necrosis factor (TNF)-α and interleukin (IL)-1β is a reliable mark for improving the prognosis. Protein kinase B (Akt) plays an important role in the development and progression of myocarditis. The specific role of the natural inhibitor of Akt, Deguelin, on myocarditis has not been reported. In this study, we used deguelin to investigate the effects of natural Akt inhibitor on myocarditis in experimental autoimmune myocarditis (EAM) rats.Materials and Methods: EAM rat models were made by using Lewis rats and Deguelin was injected intraperitoneally on day 3, 6, 9, 12 and 15 after successful modeling. On day 18, rats were sacrificed and the heart weight (HW)/ body weight (BW) ratio were measured. The pathological changes, pathological scores and fibrosis area were evaluated after H.&E. and Masson’s trichrome staining. The mRNA levels of TNF-α and IL-1β were measured by RT-qPCR, while the protein expressions of TNF-α and IL-1β were detected by immunohistochemical staining and Western bolt. The protein expressions of Akt, Akt1, phosphorylated (p-) Akt and nuclear factor (NF)-κB were detected by Western bolt.Results: We found that the TNF-α and IL-1β levels, inflammatory scores and fibrosis areas were markedly increased after 18 days deguelin administration. Conclusion: Akt inhibition with deguelin may aggravate myocarditis of EAM rats.
https://ijbms.mums.ac.ir/article_13949_082229f6b2cba5c5fa3642561367b883.pdf
2019-11-01
1275
1282
10.22038/ijbms.2019.35518.8473
Akt
Deguelin
Fibrosis
Inflammation
Myocarditis
Shanshan
Li
sharon6128126@xzhmu.edu.cn
1
Department of Forensic Medicine, Xuzhou Medical University, Xuzhou, Jiangsu 221002, China
AUTHOR
Yue
Wang
wang7459956476@163.com
2
Department of Forensic Medicine, Xuzhou Medical University, Xuzhou, Jiangsu 221002, China
AUTHOR
Chunming
Zhao
chunmingxinxiang@163.com
3
Human anatomy and Histology and Embryology, Xuzhou Medical University, Xuzhou, Jiangsu 221002, China
AUTHOR
Meixiang
Zhang
1312660812@qq.com
4
Department of Forensic Medicine, Xuzhou Medical University, Xuzhou, Jiangsu 221002, China
AUTHOR
Wei
Wang
820038790@qq.com
5
Department of Forensic Medicine, Xuzhou Medical University, Xuzhou, Jiangsu 221002, China
AUTHOR
Xiaowei
Yu
598356346@qq.com
6
Department of Forensic Medicine, Xuzhou Medical University, Xuzhou, Jiangsu 221002, China
AUTHOR
Jiao
Huang
240053309@qq.com
7
Department of Forensic Medicine, Xuzhou Medical University, Xuzhou, Jiangsu 221002, China
AUTHOR
Zhao
Wang
2209935754@qq.com
8
Department of Forensic Medicine, Xuzhou Medical University, Xuzhou, Jiangsu 221002, China
AUTHOR
Bo
Zhu
zhubo1000@gmail.com
9
Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts 02118, USA
AUTHOR
Cheng qian
Yin
ycq@bu.edu
10
Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts 02118, USA
AUTHOR
Hongxing
Cai
1663646918@qq.com
11
Department of Forensic Medicine, Xuzhou Medical University, Xuzhou, Jiangsu 221002, China
LEAD_AUTHOR
1. Bunu DM, Timofte CE, Ciocoiu M, Floria M, Tarniceriu CC, Barboi OB, et al. Cardiovascular manifestations of inflammatory bowel disease: Pathogenesis, diagnosis, and preventive strategies. Gastroenterol Res Pract 2019; 2019: 3012509.
1
2. Delgado-Maroto V, Falo CP, Forte-Lago I, Adan N, Morell M, Maganto-Garcia E, et al. The neuropeptide cortistatin attenuates experimental autoimmune myocarditis via inhibition of cardiomyogenic T cell-driven inflammatory responses. Br J Pharmacol 2017; 174: 267-280.
2
3. Maya Y, Werner RA, Schütz C, Wakabayashi H, Samnick S, Lapa C, et al. 11C-methionine PET of myocardial inflammation in a rat model of experimental autoimmune myocarditis. J Nucl Med 2016; 57: 1985-1990.
3
4. Wang H, Yao Q, Zhu S, Zhang G, Wang Z, Li Z, et al. The autopsy study of 553 cases of sudden cardiac death in Chinese adults. Heart Vessels 2014; 29: 486-495.
4
5. Blauwet LA, Cooper LT. Myocarditis. Prog Cardiovasc Dis 2010; 52: 274-288.
5
6. Cooper LT. Myocarditis. N Engl J Med 2009; 360: 1526-1538.
6
7. Zhang Y, Wang X, Yang H, Liu H, Lu Y, Han L, et al. Kinase AKT controls innate immune cell development and function. Immunology 2013; 140: 143-152.
7
8. Abeyrathna P, Su Y. The critical role of Akt in cardiovascular function. Vascul Pharmacol 2015; 74: 38-48.
8
9. Song C, Liu B, Xu P, Xie J, Ge X, Zhou Q, et al. Oxidized fish oil injury stress in Megalobrama amblycephala: Evaluated by growth, intestinal physiology, and transcriptome-based PI3K-Akt/NF-κB/TCR inflammatory signaling. Fish Shellfish Immunol 2018; 81:446-455.
9
10. Ersahin T, Tuncbag N, Cetin-Atalay R. The PI3K/ AKT/ mTOR interactive pathway. Mol Biosyst 2015; 11: 1946-1954..
10
11. Wang Y, Ma W, Zheng W. Deguelin, a novel anti-tumorigenic agent targeting apoptosis, cell cycle arrest and anti-angiogenesis for cancer chemoprevention. Mol Clin Oncol 2013; 1: 215-219.
11
12. Martini M, De Santis MC, Braccini L, Gulluni F, Hirsch E, et al. PI3K/ AKT signaling pathway and cancer: an updated review. Ann Med 2014; 46: 372-383.
12
13. Song Y, Ge W, Cai H. Curcumin protects mice from coxsackievirus B3-induced myocarditis by inhibiting the phosphatidylinositol 3 kinase/ Akt/ nuclear factor-κB pathway. J Cardiovasc Pharmacol Ther 2013; 18: 560-569.
13
14. Chen Z, Yang L, Liu Y, Tang A, Li X, Zhang J, et al. LY294002 and rapamycin promote coxsackievirus-induced cytopathic effect and apoptosis via inhibition of PI3K/ AKT/mTOR signaling pathway. Mol Cell Biochem 2014; 385: 169-177.
14
15. Liu HS, Zhang J, Guo JL, Lin CY, Wang ZW. Phosphoinositide 3-kinase inhibitor LY294002 ameliorates the severity of myosin-induced myocarditis in mice. Curr Res Transl Med 2016: 64: 21-27.
15
16. Gonzalez E, McGraw TE. The Akt kinases: isoform specificity in metabolism and cancer. Cell Cycle 2009;8:2502-2508.
16
17. Ouyang S, Zeng Q, Tang N, Guo H, Tang R, Yin W, et al. Akt-1 and Akt-2 differentially regulate the development of experimental autoimmune encephalomyelitis by controlling proliferation of thymus-derived regulatory T cells. J Immunol 2019; 202: 1441-1452.
17
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52
ORIGINAL_ARTICLE
WDR7 up-regulation upon knocking down of neighboring non-coding RNA using siRNAs encapsulated in polyamidoamine dendrimers
Objective(s): Breast cancer is the second leading cause of cancer death in females. Understanding molecular mechanisms in cancer cells compared with normal cells is crucial for diagnostic and therapeutic strategies. Long intergenic non-protein coding RNA, a regulator of reprogramming (lincRNA-RoR) is a noncoding RNA which initially was detected in induced pluripotent stem cells, and it has an important role in cell reprogramming and highly expressed in breast cancer cells. A key point in successful gene silencing is the usage of siRNA delivery system that is safe and efficient. Materials and Methods: In this study, the fifth-generation of PAMAM dendrimer is used as a nanocarrier for entering siRNA molecules for gene silencing of lincRNA-RoR. WDR7 is the gene encoding adjacent of lincRNA-RoR, which has an important role in apoptosis and cell cycle. Gel retardation assay was used to find the best Negative/Positive (N/P) molar charge ratio of siRNA- PAMAM transfected into MDA-MB 231 cells. MTT assay was performed 24 hr after transfection revealed the IC50 value (half maximal inhibitory concentrations) about 100 nanomolar for lincRNA-ROR siRNA.Results: The lincRNA-RoR and WDR7 gene expression changes were evaluated by real-time PCR after siRNA treatment and showed an increase in the gene expression of WDR7. Conclusion: This study showed that PAMAM dendrimer G5/ siRNA could be a useful system delivery for future gene therapy approaches.
https://ijbms.mums.ac.ir/article_13881_c2a8fd723d6beb1fe2825eb5bef64ca2.pdf
2019-11-01
1283
1287
10.22038/ijbms.2019.36135.8607
Breast Cancer
lncRNA ROR
Polyamidoamine dendrimer (PAMAM)
Transfection
WDR7
Sara
Kor
sarakor5965@gmail.com
1
Stem Cell Research Center, Golestan University of Medical Sciences, Gorgan, Iran
AUTHOR
vahid
Erfani-Moghadam
vahid.erfani@goums.ac.ir
2
Medical Cellular and Molecular Research Center, Golestan University of Medical Sciences, Gorgan, Iran
AUTHOR
Reza
Sahebi
reza_sahebi2001@yahoo.com
3
Department of Modern Sciences and Technologies, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Shabbou
Bahramian
bahramian89@yahoo.com
4
Stem Cell Research Center, Golestan University of Medical Sciences, Gorgan, Iran
AUTHOR
Mohammad
Shafiee
shafiee@goums.ac.ir
5
Stem Cell Research Center, Golestan University of Medical Sciences, Gorgan, Iran
LEAD_AUTHOR
1. Siegel RL, Miller KD, Jemal A. Cancer statistics. CA Cancer J Clin2017; 67:7-30.
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2. Takahashi K, Tanabe K, Ohnuki M, Narita M, Ichisaka T, Tomoda K, et al. Induction of pluripotent stem cells from adult human fibroblasts by defined factors. Cell 2007; 131:861-872.
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3. Sahebi R, Malakootian M, Balalaee B, Shahryari A, Khoshnia M, Abbaszadegan MR, et al. Linc-ROR and its spliced variants 2 and 4 are significantly up-regulated in esophageal squamous cell carcinoma. Iran J Basic Med Sci 2016; 19:1131-1135.
3
4. Wang Y, Xu Z, Jiang J, Xu C, Kang J, Xiao L, et al. Endogenous miRNA sponge lincRNA-RoR regulates Oct4, Nanog, and Sox2 in human embryonic stem cell self-renewal. Dev Cell 2013; 25:69-80.
4
5. Loewer S, Cabili MN, Guttman M, Loh Y-H, Thomas K, Park IH, et al. Large intergenic non-coding RNA-RoR modulates reprogramming of human induced pluripotent stem cells. Nat Genetics 2010; 42:1113-1117.
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6. Guo L, Zhao Y, Yang S, Zhang H, Wu Q, Chen F. An integrated evolutionary analysis of miRNA–lncRNA in mammals. Mol Biol Rep 2014; 41:201-207.
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7. Xu X-D, Li K-R, Li X-M, Yao J, Qin J, Yan B. Long non-coding RNAs: new players in ocular neovascularization. Mol Biol Rep 2014; 41:4493-4505.
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8. Rao AKDM, Rajkumar T, Mani S. Perspectives of long non-coding RNAs in cancer. Mol Biol Rep 2017; 44:203-218.
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9. Batista PJ, Chang HY. Long noncoding RNAs: cellular address codes in development and disease. Cell 2013; 152:1298-1307.
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10. Shi X, Sun M, Liu H, Yao Y, Song Y. Long non-coding RNAs: a new frontier in the study of human diseases. Cancer Lett 2013; 339:159-166.
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11. Zhan H-x, Wang Y, Li C, Xu J-w, Zhou B, Zhu J-k, et al. LincRNA-ROR promotes invasion, metastasis and tumor growth in pancreatic cancer through activating ZEB1 pathway. Cancer Lett 2016; 374:261-271.
11
12. Zhang A, Zhou N, Huang J, Liu Q, Fukuda K, Ma D, et al. The human long non-coding RNA-RoR is a p53 repressor in response to DNA damage. Cell Res 2013; 23:340-350.
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13. Guttman M, Donaghey J, Carey BW, Garber M, Grenier JK, Munson G, et al. lincRNAs act in the circuitry controlling pluripotency and differentiation. Nature 2011; 477:295-300.
13
14. Yang P, Yang Y, An W, Xu J, Zhang G, Jie J, et al. The long non‐coding RNA‐ROR promotes the resistance of radiotherapy for human colorectal cancer cells by targeting the P53/miR‐145 pathway. J Gastroenterol Hepato 2017; 32:837-845.
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15. Eades G, Wolfson B, Zhang Y, Li Q, Yao Y, Zhou Q. lincRNA-RoR and miR-145 regulate invasion in triple-negative breast cancer via targeting ARF6. Molecular Cancer Res 2015; 13:330-338.
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16. Chen Y-M, Liu Y, Wei H-Y, Lv K-Z, Fu P. Linc-ROR induces epithelial-mesenchymal transition and contributes to drug resistance and invasion of breast cancer cells. Tumor Biol 2016; 37:10861-10870.
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17. Hou P, Zhao Y, Li Z, Yao R, Ma M, Gao Y, et al. LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis. Cell Death Dis 2014; 5:e1287.
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18. Takahashi K, Yan IK, Haga H, Patel T. Modulation of hypoxia-signaling pathways by extracellular linc-RoR. J Cell Sci 2014; 127:1585-1594.
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19. Takahashi K, Yan IK, Kogure T, Haga H, Patel T. Extracellular vesicle‐mediated transfer of long non‐coding RNA ROR modulates chemosensitivity in human hepatocellular cancer. FEBS Open Bio 2014; 4:458-467.
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20. Zhou X, Gao Q, Wang J, Zhang X, Liu K, Duan Z. Linc-RNA-RoR acts as a “sponge” against mediation of the differentiation of endometrial cancer stem cells by microRNA-145. Gynecol oncol 2014; 133:333-339.
20
21. Rezaei M, Emadi-Baygi M, Hoffmann MJ, Schulz WA, Nikpour P. Altered expression of LINC-ROR in cancer cell lines and tissues. Tumor Biol 2016; 37:1763-1769.
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22. Liu Xx, Rocchi P, Qu Fq, Zheng Sq, Liang Zc, Gleave M, et al. PAMAM dendrimers mediate siRNA delivery to target Hsp27 and produce potent antiproliferative effects on prostate cancer cells. Chem Med Chem 2009; 4:1302-1310.
22
23. Perez A, Romero E, Morilla M. Ethylendiamine core PAMAM dendrimers/siRNA complexes as in vitro silencing agents. Int J Pharm 2009; 380:189-200.
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24. Merkulova M, Păunescu TG, Azroyan A, Marshansky V, Breton S, Brown D. Mapping the H (+)(V)-ATPase interactome: identification of proteins involved in trafficking, folding, assembly and phosphorylation. Sci Rep 2014; 5:14827-14827.
24
25. Sanders S, Keck-Waggoner C, Zimonjic D, Popescu N, Thorgeirsson S. Assignment1 of WDR7 (alias TRAG, TGF-β resistance associated gene) to orthologous regions of human chromosome 18q21. 1→ q22 and mouse chromosome 18D. 1–E. 3 by fluorescence in situ hybridization. Cytogenet Genome Res 2000; 88:324-325.
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26. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2− ΔΔCT method. Methods 2001; 25:402-408.
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27. Kreso A, Dick JE. Evolution of the cancer stem cell model. Cell stem cell 2014; 14:275-291.
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28. Korkaya H, Liu S, Wicha MS. Breast cancer stem cells, cytokine networks, and the tumor microenvironment. J Clin Invest 2011; 121:3804-3809.
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29. Nagano T, Fraser P. No-nonsense functions for long noncoding RNAs. Cell 2011; 145:178-181.
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30. Wu J, Huang W, He Z. Dendrimers as carriers for siRNA delivery and gene silencing: a review. Sci World J 2013; 2013.
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31. Gallas A, Alexander C, Davies MC, Puri S, Allen S. Chemistry and formulations for siRNA therapeutics. Chem Soc Rev 2013; 42:7983-7997.
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32. LiD R. WD-repeatproteins: Structurecharacteristics, biologicalfunction, and their involvement in human diseases. Cell Mol Life Sci 2001; 58:2085-2097.
32
33. Villegas VE, Zaphiropoulos PG. Neighboring gene regulation by antisense long non-coding RNAs. Int J Mol Sci 2015; 16:3251-3266.
33
ORIGINAL_ARTICLE
Metabolomics approach reveals urine biomarkers and pathways associated with the pathogenesis of lupus nephritis
Objective(s): lupus nephritis (LN) is a severe form of systemic lupus erythematosus (SLE) with renal complications. Current diagnosis is based on invasive renal biopsy and serum antibodies and complement levels that are not specific enough. The current study aims to identify new biomarker candidates for non-invasive diagnosis of LN and explore the pathogenic mechanisms that contribute to renal injury. Materials and Methods: A metabolomics approach using 1H-nuclear magnetic resonance (1H-NMR), was developed for comparison of urine metabolic profile of 14 LN patients, 10 SLE patients, and 11 healthy controls (HCs). Differential biomarker candidates were identified by using multivariate modeling, and their diagnostic accuracy was evaluated by receiver operating characteristic analysis (ROC). Results: Three metabolites were common in differentiating all three groups including beta-alanine, 2,2-dimethylsucssinic acid, and 3,4-Dihydroxyphenylacetaldehyde and suggested as a diagnostic panel for LN with AUC of 0.89, sensitivity of 81 %, and specificity of 100 %. Complementary analyses on pathways indicated that nicotinate and nicotinamide metabolism is the most important perturbed pathway in LN.Conclusion: Metabolomics is a useful tool for identification of biomarkers with the ability to diagnose LN patients and predict perturbed pathways responsible for renal injury.
https://ijbms.mums.ac.ir/article_13932_02d68c6af0b4cbbe0e6c57aa099d75ae.pdf
2019-11-01
1288
1295
10.22038/ijbms.2019.38713.9178
Biomarker
Lupus nephritis
Metabolomics
Non-invasive diagnosis
Nuclear magnetic resonance
Urinary metabolites
Shiva
Kalantari
shiva.kalantari@sbmu.ac.ir
1
Chronic Kidney Disease Research Center, Shahid Beheshti University of Medical Sciences, Tehran-Iran
AUTHOR
Saeed
Chashmniam
cheshmniyam_said@ch.sharif.edu
2
Department of Chemistry, Sharif University of Technology, Tehran, Iran
AUTHOR
Mohsen
Nafar
mohsen.nafar.sbmu@gmail.com
3
Urology-Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Zahra
Zakeri
zah_zakeri@yahoo.com
4
Department of Rheumatology, Shahid Labbafinejad Medical Center, Shahid Beheshti University of Medical Sciences Tehran, Iran
AUTHOR
Mahmoud
Parvin
m.parvin.sbmu@gmail.com
5
Department of Pathology, Shahid Labbafinejad Medical Center, Shahid Beheshti University of Medical Sciences Tehran, Iran
AUTHOR
1. Chen Y, Sun J, Zou K, Yang Y, Liu G. Treatment for lupus nephritis: an overview of systematic reviews and meta-analyses. Rheumatol Int 2017; 37:1089-1099.
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2. Chambers SA, Allen E, Rahman A, Isenberg D. Damage and mortality in a group of British patients with systemic lupus erythematosus followed up for over 10 years. Rheumatology 2009; 48:673-675.
2
3. Borchers AT, Leibushor N, Naguwa SM, Cheema GS, Shoenfeld Y, Gershwin ME. Lupus nephritis: a critical review. Autoimmun Rev 2012; 12:174-194.
3
4. Mok CC. Biomarkers for lupus nephritis: a critical appraisal. J Biomed Biotechnol 2010; 2010:638413-638424.
4
5. Lech M, Anders H-J. The pathogenesis of lupus nephritis. J Am Soc Nephrol 2013; 24:1357-1366.
5
6. Musa R, Qurie A. Lupus Nephritis. StatPearls [Internet]: StatPearls Publishing; 2018.
6
7. Rahman A, Isenberg DA. Systemic lupus erythematosus. N Engl J Med 2008; 358:929-939.
7
8. Bengtsson AA, Trygg J, Wuttge DM, Sturfelt G, Theander E, Donten M, et al. Metabolic profiling of systemic lupus erythematosus and comparison with primary Sjögren’s syndrome and systemic sclerosis. PLoS One 2016; 11:159384-159399.
8
9. Weening JJ, D’agati VD, Schwartz MM, Seshan SV, Alpers CE, Appel GB, et al. The classification of glomerulonephritis in systemic lupus erythematosus revisited. Kidney Int 2004; 65:521-530.
9
10. Romick-Rosendale LE, Brunner HI, Bennett MR, Mina R, Nelson S, Petri M, et al. Identification of urinary metabolites that distinguish membranous lupus nephritis from proliferative lupus nephritis and focal segmental glomerulosclerosis. Arthritis Res Ther 2011; 13:199-209.
10
11. Qi S, Chen Q, Xu D, Xie N, Dai Y. Clinical application of protein biomarkers in lupus erythematosus and lupus nephritis. Lupus 2018; 27:1582-1590.
11
12. Guleria A, Pratap A, Dubey D, Rawat A, Chaurasia S, Sukesh E, et al. NMR based serum metabolomics reveals a distinctive signature in patients with lupus nephritis. Sci Rep 2016; 6:35309-35320.
12
13. Nicholson JK, Lindon JC. Systems biology: metabonomics. Nature 2008; 455:1054-1056.
13
14. Beckonert O, Keun HC, Ebbels TM, Bundy J, Holmes E, Lindon JC, et al. Metabolic profiling, metabolomic and metabonomic procedures for NMR spectroscopy of urine, plasma, serum and tissue extracts. Nat Protoc 2007; 2:2692-2703.
14
15. Li J, Xie X, Zhou H, Wang B, Zhang M, Tang F. Metabolic profiling reveals new serum biomarkers of lupus nephritis. Lupus 2017; 26:1166-1173.
15
16. Kalantari S, Nafar M, Samavat S, Parvin M. 1 H NMR‐based metabolomics study for identifying urinary biomarkers and perturbed metabolic pathways associated with severity of IgA nephropathy: a pilot study. Magn Reson Chem 2017; 55:693-699.
16
17. Kalantari S, Nafar M, Samavat S, Parvin M, Nobakht M. GH BF, Barzi F. 1H NMR‐based metabolomics exploring urinary biomarkers correlated with proteinuria in focal segmental glomerulosclerosis: a pilot study. Magn Reson Chem 2016; 54:821-826.
17
18. Karnovsky A, Weymouth T, Hull T, Tarcea VG, Scardoni G, Laudanna C, et al. Metscape 2 bioinformatics tool for the analysis and visualization of metabolomics and gene expression data. Bioinformatics 2011; 28:373-380.
18
19. Artioli GG, Gualano B, Smith A, Stout J, Lancha Jr AH. Role of beta-alanine supplementation on muscle carnosine and exercise performance. Med Sci Sports Exerc 2010; 42:1162-1173.
19
20. Hipkiss AR, Brownson C, Carrier MJ. Carnosine, the anti-ageing, anti-oxidant dipeptide, may react with protein carbonyl groups. Mech Ageing Dev 2001; 122:1431-1445.
20
21. Peters V, Klessens CQ, Baelde HJ, Singler B, Veraar KA, Zutinic A, et al. Intrinsic carnosine metabolism in the human kidney. Amino acids 2015; 47:2541-2550.
21
22. Burckhardt BC, Lorenz J, Kobbe C, Burckhardt G. Substrate specificity of the human renal sodium dicarboxylate cotransporter, hNaDC-3, under voltage-clamp conditions. Am J Physiol Renal Physiol 2005; 288:792-799.
22
23. Pajor AM, Sun NN. Molecular cloning, chromosomal organization, and functional characterization of a sodium-dicarboxylate cotransporter from mouse kidney. Am J Physiol Renal Physiol 2000; 279:482-490.
23
24. Mandel LJ. Metabolic substrates, cellular energy production, and the regulation of proximal tubular transport. Annu Rev Physiol 1985; 47:85-101.
24
25. Hao X, Liu X, Wang W, Ren H, Xie J, Shen P, et al. Distinct metabolic profile of primary focal segmental glomerulosclerosis revealed by NMR-based metabolomics. PLoS One 2013; 8:78531-78541.
25
26. Burke WJ, Li SW, Williams EA, Nonneman R, Zahm DS. 3,4-Dihydroxyphenylacetaldehyde is the toxic dopamine metabolite in vivo: implications for Parkinson’s disease pathogenesis. Brain Res 2003; 989:205-213.
26
27. Burke WJ. 3,4-dihydroxyphenylacetaldehyde: a potential target for neuroprotective therapy in Parkinson’s disease. Curr Drug Targets CNS Neurol Disord 2003; 2:143-148.
27
28. Rees JN, Florang VR, Eckert LL, Doorn JA. Protein reactivity of 3,4-dihydroxyphenylacetaldehyde, a toxic dopamine metabolite, is dependent on both the aldehyde and the catechol. Chem Res Toxicol 2009; 22:1256-1263.
28
29. Anderson DG, Mariappan SV, Buettner GR, Doorn JA. Oxidation of 3,4-dihydroxyphenylacetaldehyde, a toxic dopaminergic metabolite, to a semiquinone radical and an ortho-quinone. J Biol Chem 2011; 286:26978-26986.
29
30. Rees JN. Protein reactivity of 3,4-dihydroxyphenylacetaldehyde,
30
an endogenous, potential neurotoxin relevant to Parkinson’s disease. Medicinal and Natural Products Chemistry The University of Iowa; 2009.
31
31. Moroni G, Novembrino C, Quaglini S, De Giuseppe R, Gallelli B, Uva V, et al. Oxidative stress and homocysteine metabolism in patients with lupus nephritis. Lupus 2010; 19:65-72.
32
32. Souliotis VL, Vougas K, Gorgoulis VG, Sfikakis PP. Defective DNA repair and chromatin organization in patients with quiescent systemic lupus erythematosus. Arthritis Res Ther 2016; 18:182-194.
33
33. Wang XD, Huang XF, Yan QR, Bao CD. Aberrant activation of the WNT/beta-catenin signaling pathway in lupus nephritis. PLoS One 2014; 9:84852-84859.
34
ORIGINAL_ARTICLE
Reactive oxygen species mediate TNF-α-induced inflammatory response in bone marrow mesenchymal cells
Objective(s): It is generally believed that the inflammatory response in bone marrow mesenchymal stem cells (BMSCs) transplantation leads to poor survival and unsatisfactory effects, and is mainly mediated by cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α). In this study, we explored the mechanisms underlying the TNF-α-induced inflammatory response in BMSCs. Materials and Methods: We treated BMSCs with TNF-α (1 and 10 ng/ml) for 5 days. The expression levels of key inflammatory mediators were evaluated by Real-time PCR. Intracellular ROS level was measured by using a 2, 7-dichlorofluorescein diacetate (DCF-DA).Results: We found that TNF-α treatment dramatically increased the expression levels of some key inflammatory mediators, including IL-6, IL-1β, IFN-γ and transforming growth factor β (TGF-β). Moreover, TNF-α induced intracellular oxidative stress by elevating intracellular reactive oxygen species (ROS) level, which is due to the increase of lipid peroxidation, the reduction of antioxidant Glutathione (GSH) levels and the inhibition of many antioxidant enzyme activities in BMSCs. Interestingly, 5 µM curcumin, a ROS scavenger, dramatically lowered the TNF-α-induced inflammatory response in BMSCs. In addition, TNF-α induced the activation of extracellular-signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK), p38 and their down-stream transcription factors nuclear factor kappa B (NF-κB) pathway.Conclusion: ROS mediated the TNF-α-induced inflammatory response via MAPK and NF-κB pathway, and may provide a novel strategy to prevent the inflammatory-dependent impairments in BMSCs.
https://ijbms.mums.ac.ir/article_13885_3503437c7566d04c5fd85c824589909b.pdf
2019-11-01
1296
1301
10.22038/ijbms.2019.37893.9006
BMSCs
Inflammation response
MAPK
NF-κB
Oxidative stress
TNF-α
Liuzhong
Wu
danceflyw@sina.com
1
Department of Periodontics, School of Stomatology, China Medical University, Liaoning Province, China
AUTHOR
Yaping
Pan
yapingpan2018@gmail.com
2
Department of Periodontics, School of Stomatology, China Medical University, Liaoning Province, China
LEAD_AUTHOR
1. Ni S, Wang D, Qiu X, Pang L, Song Z, Guo K. Bone marrow mesenchymal stem cells protect against bleomycin-induced pulmonary fibrosis in rat by activating Nrf2 signaling. Int J Clin Exp Pathol 2015; 8:7752-7761.
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2. Sullivan C, Murphy JM, Griffin MD, Porter RM, Evans CH, O’Flatharta C, et al. Genetic mismatch affects the immunosuppressive properties of mesenchymal stem cells in vitro and their ability to influence the course of collagen-induced arthritis. Arthritis Res Ther 2012; 14:R167.
2
3. Papadopoulou A, Yiangou M, Athanasiou E, Zogas N, Kaloyannidis P, Batsis I, et al. Mesenchymal stem cells are conditionally therapeutic in preclinical models of rheumatoid arthritis. Ann Rheum Dis 2012; 71:1733-1740.
3
4. Kolossov E, Bostani T, Roell W, Breitbach M, Pillekamp F, Nygren JM, et al. Engraftment of engineered ES cell-derived cardiomyocytes but not BM cells restores contractile function to the infarcted myocardium. J Exp Med 2006; 203:2315-2327.
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5. Lunde K, Solheim S, Aakhus S, Arnesen H, Abdelnoor M, Egeland T, et al. Intracoronary injection of mononuclear bone marrow cells in acute myocardial infarction. N Engl J Med 2006; 355:1199-1209.
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6. Liu XB, Jiang J, Gui C, Hu XY, Xiang MX, Wang JA. Angiopoietin-1 protects mesenchymal stem cells against serum deprivation and hypoxia-induced apoptosis through the PI3K/Akt pathway. Acta Pharmacol Sin 2008; 29:815-822.
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7. Chung JW, Choi RJ, Seo EK, Nam JW, Dong MS, Shin EM, et al. Anti-inflammatory effects of (Z)-ligustilide through suppression of mitogen-activated protein kinases and nuclear factor-kappaB activation pathways. Arch Pharm Res 2012; 35:723-732.
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10
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23
ORIGINAL_ARTICLE
Protection of BALB/c mice against pathogenic Brucella abortus and Brucella melitensis by vaccination with recombinant Omp16
Objective(s): Prevention of the globally spread zoonotic infection, brucellosis which affects an extensive range of hosts is still challenging researchers. There are no approved vaccines for the prevention of human disease and those used for animal brucellosis have adverse properties, which limit their application. We investigated the immunological and protective effects of recombinant 16 kDa outer membrane protein of Brucella abortus (Omp16) which introduced a new candidate for brucellosis subunit vaccine. Materials and Methods: Brucella Omp16 gene was cloned in pET-23a and expressed in Escherichia coli BL21 (DE3). Recombinant Omp16 (rOmp16) was purified using nickel resin and confirmed by Western blot analysis. BALB/c mice were immunized with rOmp16, afterward, specific serum antibodies and cytokine responses were evaluated. Protection of immunized mice against pathogenic B. abortus 544 and B. melitensis 16M was evaluated by the intraperitoneal bacterial challenge. Results: Sequencing results of the recombinant plasmid vector along with Western blotting confirmed the cloning procedure. Recognition of rOmp16 by specific IgG from serum samples of infected cases suggests the stimulation of immune response to this protein. Significant total serum IgG along with remarkable IgG1 and IgG2a response to the protein was recorded. A significant increase in IFN-γ, and IL-4 levels were observed from splenocyte cultures of immunized mice which were stimulated with rOmp16 suggesting the development of T-lymphocyte mediated immunity against the recombinant antigen. Conclusion: The intraperitoneal challenge with B. abortus 544 and B. melitensis 16M confirmed that rOmp16 is able to elicit efficient protective immune responses in the animal host.
https://ijbms.mums.ac.ir/article_13934_15dba482abe61a817f13091d67414971.pdf
2019-11-01
1302
1307
10.22038/ijbms.2019.36369.8665
BALB/c mice
Brucella
Brucellosis
Outer membrane protein
Recombinant protein
Hamed
Alizadeh
hamedalizadeh1986@yahoo.com
1
Department of Microbiology, Karaj Branch, Islamic Azad University, Karaj, Iran
AUTHOR
Mehrooz
Dezfulian
dezfoolian@rocketmail.com
2
Department of Microbiology, Karaj Branch, Islamic Azad University, Karaj, Iran
AUTHOR
Mehdi
Rahnema
meh_rahnema@yahoo.com
3
Department of Microbiology, Zanjan Branch, Islamic Azad University, Zanjan, Iran
AUTHOR
jalil
fallah mehrabadi
jalil.fallah@gmail.com
4
Lister Laboratory of Microbiology, Tehran, Iran
AUTHOR
Davood
Esmaeili
esm114@gmail.com
5
Department of Microbiology and Applied Microbiology Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
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25. Pasquevich KA, Estein SM, Garcia Samartino C, Zwerdling A, Coria LM, Barrionuevo P, Fossati CA, Giambartolomei GH, Cassataro J. Immunization with recombinant Brucella species outer membrane protein Omp16 or Omp19 in adjuvant induces specific CD4+ and CD8+ T cells as well as systemic and oral protection against Brucella abortus infection. Infect Immun 2009; 77:436-445.
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50
ORIGINAL_ARTICLE
Protein expression changes of HCN1 and HCN2 in hippocampal subregions of gerbils during the normal aging process
Objective(s): Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels play essential roles in various hippocampal functions, including regulation of long-term potentiation, synaptic plasticity, and hippocampal-dependent cognitive process. The objective of this study was to investigate age-related changes in HCN1 and HCN2 protein expressions in gerbil hippocampus at various ages. Materials and Methods: In this study, the protein expressions of HCN1 and HCN2 were compared in the hippocampus at the ages of 1, 3, 12, and 24 months using Western blot analysis and immunohistochemistry.Results: Immunoreactivity of both HCN1 and HCN2 was shown primarily in cells of the pyramidal cell layer in the hippocampus proper and in cells of the granule cell layer in the dentate gyrus. HCN1 and HCN2 protein expression levels and immunoreactivity were significantly increased at three months (3 M) of age compared with those at 1 M of age. After that, both HCN1 and HCN2 expression levels in the hippocampus were gradually decreased with age. Conclusion: Our results show that the normal aging process affects the expression levels of HCN1 and HCN2 in hippocampal cells in gerbils. There are marked reductions in HCN1 and HCN2 expressions in the aged hippocampus compared to the young hippocampus. Such reductions might be related to aging in the hippocampus.
https://ijbms.mums.ac.ir/article_13883_4de7a34077f6f7aa0ebac6ec33bbcdbe.pdf
2019-11-01
1308
1313
10.22038/ijbms.2019.35760.8520
Aging
Dentate gyrus
Granule cells
HCN channel
Hippocampus proper
Pyramidal cells
Choong-Hyun
Lee
anaphy@dankook.ac.kr
1
Department of Pharmacy, College of Pharmacy, Dankook University, Cheonan, Chungnam 31116, Republic of Korea
AUTHOR
Joon Ha
Park
jh-park@hallym.ac.kr
2
Department of Anatomy, College of Korean Medicine, Dongguk University, Gyeongju, Gyeongbuk 38066, Republic of Korea
AUTHOR
Moo-Ho
Won
mhwon@kangwon.ac.kr
3
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 24341, Republic of Korea
LEAD_AUTHOR
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39. Luo P, Lu Y, Li C, Zhou M, Chen C, Lu Q, et al. Long-lasting spatial learning and memory impairments caused by chronic cerebral hypoperfusion associate with a dynamic change of HCN1/HCN2 expression in the hippocampal CA1 region. Neurobiol Learn Mem 2015; 123:72-83.
39
ORIGINAL_ARTICLE
Nitric oxide mediated the effects of nebivolol in cardiorenal syndrome
Objective(s): Despite several proposed mechanisms for the pathophysiology of cardiorenal syndrome (CRS), the exact mechanism remains unclear. Nitrosative stress has been argued as a key mechanism recently. Nebivolol is a beta-blocker with nitric oxide (NO)-releasing effect. In the present study, NO-mediated effects of two different treatment regimes of nebivolol in CRS were studied. Materials and Methods: Rats were divided into: sham-operated (sham-control), myocardial infarction (MI)-induced, (MI-control) early nebivolol-treated (MI-neb1) and late nebivolol-treated (Mı-neb2) groups. The effects of nebivolol were assessed both in the early and late period of MI by histologic, hemodynamic and biologic studies.Results: Developed MI model was in line with the heart failure with preserved ejection fraction. Focal and total tubular damage findings were observed in MI-control group both in early and late period of MI. In parallel, subclinical functional damage was transformed into chronic renal dysfunction in this group. Increased inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) together with decreased neuronal NOS (nNOS) levels were in parallel with the increased inflammation and nitrosative stress biomarkers. Nebivolol effectively prevented both subclinical and clinical nephropathy. There was no statistical difference between the nebivolol treatment regimes.Conclusion: The beneficial effects of nebivolol were closely related to the reduction of nitrosative damages as well as hemodynamic alterations. The NO-mediated effects were: prevention of nitrosative damage by decreasing iNOS, preservation of nNOS in order to maintain glomerular filtration rate (GFR), and restoration of eNOS in the late period of MI. On contrary to our previous work, early nebivolol administration had a similar effect with delayed administration of nebivolol on CRS.
https://ijbms.mums.ac.ir/article_13879_ace2e3a1f1e612d6c09f6b763d066758.pdf
2019-11-01
1314
1324
10.22038/ijbms.2019.37400.8927
Cardiorenal syndrome
Myocardial infarction
Nebivolol
Nitric oxide
Nitrosative damage
Guldem
Mercanoglu
guldemiko@gmail.com
1
University of Health Sciences, Faculty of Pharmacy, Department of Pharmacology, Istanbul-Turkey
LEAD_AUTHOR
Semen
Onder
syesil@gmail.com
2
Istanbul University, Istanbul Medical Faculty, Department of Pathology, Istanbul-Turkey
AUTHOR
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52
ORIGINAL_ARTICLE
Association of lipid markers with coronary heart disease and stroke mortality: A 15-year follow-up study
Objective(s): It has been proposed that lipid markers may predict cardiovascular events; however, their effect may vary depending on the type of cardiovascular disease. The purpose of this study was to investigate the effects of lipid markers on death from coronary heart disease (CHD) and stroke in competing risks setting.Materials and Methods: Participants included 2502 women and 2020 men, age 40 years or older from Tehran Lipid and Glucose Study. The association between total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), and high-density lipoprotein cholesterol (HDL-C) with hazard and cumulative incidence of CHD and stroke was investigated using cause-specific hazard and sub-distribution hazard models. Statistical analyses were performed using “risk regression” and “cmprsk” package in R 3.3.2.Results: One standard deviation (SD) increase in TC and LDL-C increased the hazard of CHD death by 1.42 (CI=1.07,1.89) and 1.41 (CI=1.04,1.93), respectively. 1-SD increase in TG increased the cumulative incidence of CHD death increased by 1.94 (CI=1.02,3.75) in women. Other risk factors were not associated with the hazard and cumulative incidence of CHD in women, men and the total sample. In addition, none of lipids had a significant effect on the hazard and cumulative incidence of stroke in men, women and the total sample.Conclusion: The associations of lipid components on CHD death were modified by gender. TC, LDL-C and TG were independent predictors of CHD mortality in women. Furthermore, death due to stroke changes the association of lipid markers with CHD mortality.
https://ijbms.mums.ac.ir/article_13884_604aef9eb4cb80e515bb8cacc3487ad9.pdf
2019-11-01
1325
1330
10.22038/ijbms.2019.35617.8775
Coronary Heart Disease
Cholesterol HDL
Cholesterol LDL
Stroke
Survival analysis
Bagher
Pahlavanzade
db.pahlavan@gmail.com
1
Departments of Biostatistics, Faculty of Paramedical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Farid
Zayeri
farid.zayeri1@gmail.com
2
Departments of Biostatistics, Faculty of Paramedical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Taban
Baghfalaki
t.baghfalaki1@gmail.com
3
Departments of Statistics, Faculty of Mathematical Sciences, Tarbiat Modares University, Tehran, Iran
AUTHOR
Omid
Mozafari
badl.mt842@gmail.com
4
Golestan University of Medical Sciences, Gorgan, Iran
AUTHOR
Davood
Khalili
khalilidavood269@gmail.com
5
Prevention of Metabolic Disorders Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Fereidoun
Azizi
fereidon.azizy@gmail.com
6
Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Alireza
Abadi
alireza.abadi308@gmail.com
7
Department of Community Medicine, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1. Organization WH. Cardiovascular disease, On World Heart Day WHO calls for accelerated action to prevent the world’s leading global killer 2018. Available from: http://www.who.int/cardiovascular_diseases/en/.
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2. Benjamin EJ, Virani SS, Callaway CW, Chamberlain AM, Chang AR, Cheng S, et al. Heart disease and stroke statistics—2018 update: a report from the American Heart Association. Circulation 2018; 137:e67-e492.
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5. Canouï-Poitrine F, Luc G, Bard J-M, Ferrieres J, Yarnell J, Arveiler D, et al. Relative contribution of lipids and apolipoproteins to incident coronary heart disease and ischemic stroke: the PRIME Study. Cerebrovascular Diseases 2010; 30:252-259.
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6. Iso H, Sato S, Kitamura A, Imano H, Kiyama M, Yamagishi K, et al. Metabolic syndrome and the risk of ischemic heart disease and stroke among Japanese men and women. Stroke 2007; 38:1744-1751.
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7. Tohidi M, Mohebi R, Cheraghi L, Hajsheikholeslami F, Aref S, Nouri S, et al. Lipid profile components and incident cerebrovascular events versus coronary heart disease; the result of 9 years follow-up in Tehran Lipid and Glucose Study. Clin Biochem 2013; 46:716-721.
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8. Tsukinoki R, Okamura T, Watanabe M, Kokubo Y, Higashiyama A, Nishimura K, et al. Blood pressure, low-density lipoprotein cholesterol, and incidences of coronary artery disease and ischemic stroke in Japanese: the Suita study. Am J Hypertens 2014; 27:1362-1369.
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9. Puddu PE, Piras P, Menotti A. Lifetime competing risks between coronary heart disease mortality and other causes of death during 50 years of follow-up. Int J Cardiol 2017; 228:359-363.
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10. Liu L, Tang Z, Li X, Luo Y, Guo J, Li H, et al. A novel risk score to the prediction of 10-year risk for coronary artery disease among the elderly in Beijing based on competing risk model. Medicine 2016; 95.
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11. Puddu PE, Piras P, Menotti A. Competing risks and lifetime coronary heart disease incidence during 50 years of follow-up. Int J Cardiol 2016; 219:79-83.
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12. Prugger C, Wellmann J, Heidrich J, Brand-Herrmann S-M, Keil U. Cardiovascular risk factors and mortality in patients with coronary heart disease. Eur J Epidemiol 2008; 23:731.
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13. National Institute of Health DoHaHS. Coronary Heart Disease Risk Factors 2018. Available from: https://www.nhlbi.nih.gov/health-topics/coronary-heart-disease-risk-factors.
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14. Amarenco P, Labreuche J, Touboul P-J. High-density lipoprotein-cholesterol and risk of stroke and carotid atherosclerosis: a systematic review. Atherosclerosis 2008; 196:489-496.
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15. Overvad TF, Nielsen PB, Larsen TB, Søgaard P. Left atrial size and risk of stroke in patients in sinus rhythm. Thromb Haemost 2016; 116:206-219.
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16. Everett BM, Kurth T, Buring JE, Ridker PM. The relative strength of C-reactive protein and lipid levels as determinants of ischemic stroke compared with coronary heart disease in women. J Am Coll Cardiol 2006; 48:2235-2242.
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17. Glynn RJ, Rosner B. Comparison of risk factors for the competing risks of coronary heart disease, stroke, and venous thromboembolism. Am J Epidemiol 2005; 162:975-982.
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18. Hamer M, Batty GD, Stamatakis E, Kivimaki M. Comparison of risk factors for fatal stroke and ischemic heart disease: A prospective follow up of the health survey for England. Atherosclerosis 2011; 219:807-810.
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19. Sadeghpour S, Faghihimani E, Hassanzadeh A, Amini M, Mansourian M. Predictors of all-cause and cardiovascular-specific mortality in type 2 diabetes: A competing risk modeling of an Iranian population. Adv Biomed Res 2016; 5:82.
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20. Patterson CC, Blankenberg S, Ben-Shlomo Y, Heslop L, Bayer A, Lowe G, et al. Troponin and BNP are markers for subsequent non-ischaemic congestive heart failure: the Caerphilly Prospective Study (CaPS). Open heart 2018; 5:e000692.
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21. Latouche A, Allignol A, Beyersmann J, Labopin M, Fine JP. A competing risks analysis should report results on all cause-specific hazards and cumulative incidence functions. J Clin Epidemiol 2013; 66:648-653.
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22. Azizi F, Madjid M, Rahmani M, Emami H, Mirmiran P, Hadjipour R. Tehran Lipid and Glucose Study (TLGS): rationale and design. Iranian journal of endocrinology and metabolism 2000; 2:77-86.
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23. Tohidi M, Hatami M, Hadaegh F, Safarkhani M, Harati H, Azizi F. Lipid measures for prediction of incident cardiovascular disease in diabetic and non-diabetic adults: results of the 8.6 years follow-up of a population based cohort study. Lipids Health Dis 2010; 9:6.
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24. Azizi F, Ghanbarian A, Momenan AA, Hadaegh F, Mirmiran P, Hedayati M, et al. Prevention of non-communicable disease in a population in nutrition transition: Tehran Lipid and Glucose Study phase II. Trials 2009; 10:5.
24
25. Azizi F, Rahmani M, Emami H, Mirmiran P, Hajipour R, Madjid M, et al. Cardiovascular risk factors in an Iranian urban population: Tehran lipid and glucose study (phase 1). Soz Praventivmed 2002; 47:408-426.
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26. Dianatkhah M, Rahgozar M, Talaei M, Karimloua M, Sadeghi M, Oveisgharan S, et al. Comparison of competing risks models based on cumulative incidence function in analyzing time to cardiovascular diseases. ARYA Atheroscler 2014; 10:6-12.
26
27. Peters SA, Singhateh Y, Mackay D, Huxley RR, Woodward M. Total cholesterol as a risk factor for coronary heart disease and stroke in women compared with men: A systematic review and meta-analysis. Atherosclerosis 2016; 248:123-131.
27
ORIGINAL_ARTICLE
Potential therapeutic effect of Moroccan propolis in hyperglycemia, dyslipidemia, and hepatorenal dysfunction in diabetic rats
Objective(s): The effect of propolis collected in Morocco on blood glucose, lipid profile, liver enzymes, and kidney function was investigated in control and diabetic rats. Materials and Methods: Antioxidant activity of propolis was evaluated with the use of DPPH, 2,2’-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) (ABTS•+), ferric reducing power and total antioxidant activity assay. To study its effect in streptozotocin (STZ)-induced diabetes, the rats were divided into eight groups; four control and four diabetics. The animals received distilled water, glibenclamide, or propolis extract, 50 mg/kg/BW) or 100 mg/kg/b.wt, daily for 15 days. Blood glucose, triglyceride, lactic acid dehydrogenase, liver enzymes, creatinine, blood urea, lipid profile, and body weight were measured on day 15 after commencement of the treatment. Results: Propolis has a strong antioxidant activity and high total flavonoids and polyphenols content. Glibenclamide and propolis have no significant effect on lipid parameters, and renal and hepatic function in non-diabetic rats. However, propolis or glibenclamide caused a significant lowering of blood glucose after a single administration and at day 15 after daily administration in diabetic rats (P<0.05). Both interventions significantly lowered lactic acid dehydrogenase, increased body weight, and ameliorated dyslipidemia and abnormal liver and kidney function caused by diabetes. The effect of propolis was dose-dependent and in a high dose it was more potent than glibenclamide. Conclusion: Propolis exhibited strong antihyperglycemic, antihyperlipidemic, and hepato-renal protective effects in diabetes, and significantly lowered the elevated lactic acid dehydrogenase. The study demonstrated for the first-time the effect of Moroccan propolis in diabetes and it will pave the way for clinical investigations.
https://ijbms.mums.ac.ir/article_13937_26d6ad8912ff23beaa4d9f61c4e97dfa.pdf
2019-11-01
1331
1339
10.22038/ijbms.2019.33549.8004
Antioxidant
Diabetes
Kidney
Liver
Propolis
Nawal
El Menyiy
nawal.55@hotmail.com
1
Laboratory Physiology-Pharmacology & Environmental Health, Faculty of science Dhar El Mehraz, University Sidi Mohamed Ben Abdallah, Fez, Morocco
AUTHOR
Noori
Al-Waili
noori786@yahoo.com
2
New York Medical Care for Nephrology, New York City, NY, USA
LEAD_AUTHOR
Asmae
El Ghouizi
asmaer1@gmail.com
3
Laboratory Physiology-Pharmacology & Environmental Health, Faculty of science Dhar El Mehraz, University Sidi Mohamed Ben Abdallah, Fez, Morocco
AUTHOR
Soukaina
El-Guendouz
soukaina1@gmail.com
4
Laboratory Physiology-Pharmacology & Environmental Health, Faculty of science Dhar El Mehraz, University Sidi Mohamed Ben Abdallah, Fez, Morocco
AUTHOR
Khelod
Salom
drnoori6@yahoo.com
5
New York Medical Care for Nephrology, New York City, NY, USA
AUTHOR
Badiaa
Lyoussi
lyoussib@gmail.com
6
Laboratory Physiology-Pharmacology & Environmental Health, Faculty of science Dhar El Mehraz, University Sidi Mohamed Ben Abdallah, Fez, Morocco
AUTHOR
1. Al-Waili N, Al-Waili H, Al-Waili T, Salom K. Natural antioxidants in the treatment and prevention of diabetic nephropathy; a potential approach that warrants clinical trials. Redox Rep 2017; 22:99-118.
1
2. Kumazawa S, Hamasaka T, Nakayama T. Antioxidant activity of propolis of various geographic origins. Food Chem 2004; 84:329-339.
2
3. Al Ghamdi AA, Badr G, Hozzein WN, Allam A, Al-Waili NS, Al-Wadaan MA, et al. Oral supplementation of diabetic mice with propolis restores the proliferation capacity and chemotaxis of B and T lymphocytes towards CCL21 and CXCL12 by modulating the lipid profile, the pro-inflammatory cytokine levels and oxidative stress. BMC Immunol 2015; 16:54-68.
3
4. Al-Waili N, Al-Ghamdi A, Ansari MJ. Synergistic effects of honey and propolis toward drug multi-resistant Staphylococcus aureus, Escherichia coli and Candida albicans isolates in single and polymicrobial cultures. Int J Med Sci 2012; 9:793-800.
4
5. El-Guendouz S, Al-Waili N, Aazza S, Elamine Y, Zizi S, Al-Waili T, et al. Antioxidant and diuretic activity of co-administration of Capparis spinosa honey and propolis in comparison to furosemide. Asian Pac J Trop Med 2017; 10:974-980.
5
6. Valenzuela-Barra G, Castro C, Figueroa C, Barriga A, Silva X, Heras B, et al. Anti-inflammatory activity and phenolic profile of propolis from two locations in Región Metropolitana de Santiago, Chile. J Ethnopharmacol 2015; 26:37-44.
6
7. Silva-Carvalho R, Miranda-Gonçalves V , Ferreira A, Cardoso S, Sobral A, Almeida-Aguiar C , et al. Antitumoural and antiangiogenic activity of Portuguese propolis in in vitro and in vivo models. J functional foods 2014; 11:160-171.
7
8. El Menyiy N, Al Waili N, Bakour M, Al-Waili H, Lyoussi B. Protective effect of propolis in proteinuria, crystaluria, nephrotoxicity and hepatotoxicity induced by ethylene glycol ingestion. Arch Med Res 2016; 47:526-534.
8
9 . Hu F, Hepburn H, Xuan H, Chen M, Daya S, Radloff S. Effects of propolis on blood glucose, blood lipid and free radicals in rats with diabetes mellitus. Pharmacol Res 2005; 51:147-152.
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10. Al-Hariri M, Eldin T, Abu-Hozaifa B, Elnour A. Glycemic control and anti-osteopathic effect of propolis in diabetic rats. Diabetes Metab Syndr Obes 2011; 4:377-384.
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63
ORIGINAL_ARTICLE
Eupafolin ameliorates lipopolysaccharide-induced cardiomyocyte autophagy via PI3K/AKT/mTOR signaling pathway
Objective(s): Eupafolin, a major active component of Eupatorium perfoliatum L., has anti-inflammatory and anti-oxidant properties. Lipopolysaccharide (LPS) is responsible for myocardial depression. A line of evidences revealed that LPS induces autophagy in cardiomyocytes injury. This study aims to evaluate the effects of eupafolin on LPS-induced cardiomyocyte autophagy. Materials and Methods: The effect of LPS on cell viability was examined by CCK-8. Autophagic protein 2 light chain 3 (LC3II), which was regulated by LPS and eupafolin, was examined using immunofluorescent staining. The expression levels of Beclin-1 and p62 were detected by western blotting. The effects of eupafolin on phosphatidylinositol-3-kinase/ protein kinase B/ mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway were also evaluated by western blotting and immunofluorescent staining. Results: Eupafolin pretreatment reduced the expression of LC3II and Beclin-1, whereas p62 was significant increased. In addition, eupafolin promoted expression of PI3K/AKT/mTOR signaling pathway and mTOR inhibitor rapamycin reversed the inhibitory effects on LPS-induced cardiomyocyte autophagy. Conclusion: Eupafolin exerts anti-autophagy activity via activation of PI3K/AKT/mTOR signaling pathway.
https://ijbms.mums.ac.ir/article_13948_c7cd344cbc086e0540602101d7869527.pdf
2019-11-01
1340
1346
10.22038/ijbms.2019.37748.8977
Autophagy
Cardiomyocyte
Eupafolin
Lipopolysaccharides
Mammalian target of rapamycin
Yan
Gao
caoruiyun_bd@126.com
1
Function Testing Lab, Shaanxi Provincial People’s Hospital, Xi’an, Shaanxi P.R. China
LEAD_AUTHOR
Yi
Zhang
13891907930@163.com
2
ICU Department, Shaanxi Provincial People’s Hospital. Xi’an, Shaanxi P.R. China
AUTHOR
Yangyang
Fan
314520356@qq.com
3
Obstetrical Department, Shaanxi Provincial People’s Hospital. Xi’an, Shaanxi P.R. China
AUTHOR
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ORIGINAL_ARTICLE
Contribution of potassium channels, beta2-adrenergic and histamine H1 receptors in the relaxant effect of baicalein on rat tracheal smooth muscle
Objective(s): Baicalein, a compound extracted from a variety of herbs, showed various pharmacological effects. This study evaluated the relaxant effects of baicalein and its underlying molecular mechanisms of action on rat’s isolated tracheal smooth muscle.Materials and Methods: Tracheal smooth muscle were contracted by 10 μM methacholine or 60 mM KCl and the effects of cumulative concentrations of baicalein (5, 10, 20 and 40 mg/ml) and theophylline (0.2, 0.4, 0.6 and 0.8 mM) were evaluated. To examine the possible mechanism(s) of the relaxant effect of baicalein, its effect was also evaluated on incubated tissues with atropine, indomethacin, diltiazem, N(G)-Nitro-L-arginine methyl ester (L-NAME), glibenclamide, propranolol and chlorpheniramine.Results: A concentration-dependent and significant relaxant effect was seen for baicalein in non-incubated tissues contracted by KCl or methacholine (PConclusion: A potent relaxant effect comparable to the effect of theophylline was shown for baicalein, which was probably mediated via inhibition of histamine (H1) receptors, stimulation of beta2-adrenergic receptors and potassium channels activation.
https://ijbms.mums.ac.ir/article_13936_ed360ddb8737f76e8cfe845f2c5f2717.pdf
2019-11-01
1347
1352
10.22038/ijbms.2019.36377.8666
Baicalein
Beta2-adrenergic
Histamine H1 receptors
Relaxation
Smooth Muscle
Trachea
Saeideh
Saadat
saadats931@mums.ac.ir
1
Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Javad
Boskabadi
boskabadij901@mums.ac.ir
2
Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mohammad Hossein
Boskabady
boskabadymh@mums.ac.ir
3
Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Ajay M, Gilani A-uH, Mustafa MR. Effects of flavonoids on vascular smooth muscle of the isolated rat thoracic aorta. Life Sci 2003; 74:603-612.
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19. Chen B, Senthilkumar R, Rong F, Guo Q. Cardioprotective potential of baicalein: A short review of in vitro and in vivo studies. Pharm Anal Acta 2014; 5:280-284.
19
ORIGINAL_ARTICLE
Sodium valproate ameliorates aluminum-induced oxidative stress and apoptosis of PC12 cells
Objective(s): According to recent studies, valproate shows some protection against oxidative stress (OS) induced by neurotoxins. Current investigation tried to determine the possible ameliorating effects of sodium valproate (SV) against aluminum (Al)-induced cell death, apoptosis, mitochondrial membrane potential (MMP), and OS in PC12 cells.Materials and Methods: In this in vitro study, PC12 cells were treated with different concentrations of aluminum maltolate (Almal) with and without SV (50–400 µM). Cell viability was assessed by MTT assay. To measure quantitatively the effects of SV on Al-induced apoptosis and reactive oxygen species (ROS), flowcytometry using 7AAD/annexin-V and 2’, 7’-dichlorofluorescein diacetate staining were employed, respectively. MMP was monitored using the retention of rhodamine 123. Catalase (CAT) activity was assayed by the rate of decomposition of hydrogen peroxide. Results: Exposure of PC12 cells for 48 hr to Almal (125–2000 µM) significantly reduced cell viability (IC50=1090 μM), increased ROS generation and apoptosis, and reduced MMP and CAT activity. SV reduced the Almal-induced cell death and apoptosis. Furthermore, the effects of Almal on ROS generation, catalase activity, and MMP reduction were significantly diminished by SV. Conclusion: Data from this study suggest that SV can inhibit Al-induced cell death and apoptosis of PC12 cells via ameliorating OS.
https://ijbms.mums.ac.ir/article_13950_7e2525fa4213f1e5c34895fb36212f93.pdf
2019-11-01
1353
1358
10.22038/ijbms.2019.36930.8804
Aluminum maltolate
Apoptosis
Histone deacetylase inhibitor
Oxidative stress
Valproic acid
Forough
Iranpak
forough.iranpak@yahoo.com
1
Department of Biochemistry, Islamic Azad University of Shiraz, Shiraz, Iran
AUTHOR
Jamileh
Saberzadeh
j.saberzadeh@gmail.com
2
Diagnostic Laboratory Sciences and Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Mahmood
Vesal
vesalm@sums.ac.ir
3
Department of Biochemistry, Islamic Azad University of Shiraz, Shiraz, Iran
AUTHOR
Mohammad Ali
Takhshid
takhshid2001@yahoo.co.uk
4
Diagnostic Laboratory Sciences and Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
LEAD_AUTHOR
1. Klotz K, Weistenhofer W, Neff F, Hartwig A, van Thriel C, Drexler H. The health effects of aluminum exposure. Dtsch Arztebl Int 2017; 114:653-659.
1
2. Farhat SM, Mahboob A, Iqbal G, Ahmed T. Aluminum-induced cholinergic deficits in different brain parts and its implications on sociability and cognitive functions in mouse. Biol Trace Elem Res 2017; 177:115-121.
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3. Kaur A, Gill KD. Disruption of neuronal calcium homeostasis after chronic aluminium toxicity in rats. Basic Clin Pharmacol Toxicol 2005; 96:118-122.
3
4. Saberzadeh J, Arabsolghar R, Takhshid MA. Alpha synuclein protein is involved in Aluminum-induced cell death and oxidative stress in PC12 cells. Brain Res 2016; 1635:153-160.
4
5. Sakamoto T, Saito H, Ishii K, Takahashi H, Tanabe S, Ogasawara Y. Aluminum inhibits proteolytic degradation of amyloid beta peptide by cathepsin D: a potential link between aluminum accumulation and neuritic plaque deposition. FEBS Lett 2006; 580:6543-6549.
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6. Aremu DA, Ezomo OF, Meshitsuka S. Gene expression in primary cultured astrocytes affected by aluminum: alteration of chaperons involved in protein folding. Environ Health Prev Med 2011; 16:16-24.
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7. Rizvi SH, Parveen A, Ahmad I, Ahmad I, Verma AK, Arshad M, et al. Aluminum activates PERK-EIF2alpha signaling and inflammatory proteins in human neuroblastoma SH-SY5Y Cells. Biol Trace Elem Res 2016; 172:108-119.
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8. Yuan CY, Lee YJ, Hsu GS. Aluminum overload increases oxidative stress in four functional brain areas of neonatal rats. J Biomed Sci 2012; 19:51.
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9. Esparza JL, Gomez M, Domingo JL. Role of melatonin in aluminum-related neurodegenerative disorders: A review. Biol Trace Elem Res 2019;188:60-67.
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11. Wei Y, Liu D, Zheng Y, Li H, Hao C, Ouyang W. Protective effects of kinetin against aluminum chloride and D-galactose induced cognitive impairment and oxidative damage in mouse. Brain Res Bull 2017; 134:262-272.
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12. Filakovic P, Eric AP. Pharmacotherapy of suicidal behaviour in major depression, schizophrenia and bipolar disorder. Coll Antropol 2013; 37:1039-1044.
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13. Afzal E, Alinezhad S, Khorsand M, Khoshnood MJ, Takhshid MA. Effects of two-by-two combination therapy with valproic acid, lithium chloride, and celecoxib on the angiogenesis of the chicken chorioallantoic membrane. Iran J Med Sci 2018; 3:506-513.
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14. Fanian M, Bahmani M, Mozafari M, Naderi S, Alizadeh Zareie M, Okhovat MA, et al. The synergistic effects of celecoxib and sodium valproate on apoptosis and invasiveness behavior of papillary thyroid cancer cell line in-vitro. Iran J Pharm Res 2018; 7:1008-1017.
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15. Damaskos C, Valsami S, Kontos M, Spartalis E, Kalampokas T, Kalampokas E, et al. Histone deacetylase inhibitors: An attractive therapeutic strategy against breast cancer. Anticancer Res 2017; 37:35-46.
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16. Lee TB, Moon YS, Choi CH. Histone H4 deacetylation down-regulates catalase gene expression in doxorubicin-resistant AML subline. Cell Biol Toxicol 2012; 28:11-18.
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17. Zhang Z, Qin X, Zhao X, Tong N, Gong Y, Zhang W, et al. Valproic acid regulates antioxidant enzymes and prevents ischemia/reperfusion injury in the rat retina. Curr Eye Res 2012; 37:429-437.
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18. Saberzadeh J, Omrani M, Takhshid MA. Protective effects of nimodipine and lithium against aluminum-induced cell death and oxidative stress in PC12 cells. Iran J Basic Med Sci 2016; 19:1251-1257.
18
19. Shokoohinia Y, Khajouei S, Ahmadi F, Ghiasvand N, Hosseinzadeh L. Protective effect of bioactive compounds from Echinophora cinerea against cisplatin-induced oxidative stress and apoptosis in the PC12 cell line. Iran J Basic Med Sci 2017; 20:438-445.
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22. Silva MR, Correia AO, Dos Santos GCA, Parente LLT, de Siqueira KP, Lima DGS, et al. Neuroprotective effects of valproic acid on brain ischemia are related to its HDAC and GSK3 inhibitions. Pharmacol Biochem Behav 2018; 167:17-28.
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24. Peng GS, Li G, Tzeng NS, Chen PS, Chuang DM, Hsu YD, et al. Valproate pretreatment protects dopaminergic neurons from LPS-induced neurotoxicity in rat primary midbrain cultures: role of microglia. Brain Res Mol Brain Res 2005; 134:162-169.
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26. Wang C, Wang Y, Qiao Z, Kuai Q, Wang Y, Wang X, et al. Valproic acid-mediated myocardial protection of acute hemorrhagic rat via the BCL-2 pathway. J Trauma Acute Care Surg 2016; 80:812-818.
26
27. Brest P, Lassalle S, Hofman V, Bordone O, Gavric Tanga V, Bonnetaud C, et al. MiR-129-5p is required for histone deacetylase inhibitor-induced cell death in thyroid cancer cells. Endocr Relat Cancer 2011; 18:711-719.
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28. Zhang Z, Qin X, Tong N, Zhao X, Gong Y, Shi Y, et al. Valproic acid-mediated neuroprotection in retinal ischemia injury via histone deacetylase inhibition and transcriptional activation. Exp Eye Res 2012; 94:98-108.
28
29. Jensen ML, Frongillo EA, Leroy JL, Blake CE. Participating in a food-assisted maternal and child nutrition and health program in rural guatemala alters household dietary choices. J Nutr 2016; 146:1593-1600.
29
30. Cardenas-Rodriguez N, Coballase-Urrutia E, Rivera-Espinosa L, Romero-Toledo A, Sampieri A, Ortega-Cuellar D, et al. Modulation of antioxidant enzymatic activities by certain antiepileptic drugs (valproic acid, oxcarbazepine, and topiramate): evidence in humans and experimental models. Oxid Med Cell Longev 2013; 2013:598493.
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31. Kabel AM, Omar MS, Elmaaboud MAA. Amelioration of bleomycin-induced lung fibrosis in rats by valproic acid and butyrate: Role of nuclear factor kappa-B, proinflammatory cytokines and oxidative stress. Int Immunopharmacol 2016; 39:335-342.
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32. Tokarz P, Kaarniranta K, Blasiak J. Inhibition of DNA methyltransferase or histone deacetylase protects retinal pigment epithelial cells from DNA damage induced by oxidative stress by the stimulation of antioxidant enzymes. Eur J Pharmacol 2016; 776:167-175.
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34
35. Li R, Liu Y, Chen N, Zhang Y, Song G, Zhang Z. Valproate attenuates nitroglycerin-induced trigeminovascular activation by preserving mitochondrial function in a rat model of migraine. Med Sci Monit 2016; 22:3229-3237.
35
ORIGINAL_ARTICLE
Renal histopathological and biochemical changes following adjuvant intervention of Momordica charantia and antiretroviral therapy in diabetic rats
Objective(s): Diabetic nephropathy (DN) is an important primary cause of end-stage kidney disease. This study explores the mechanisms of the reno-protective effects of Momordica charantia (M. charantia) in diabetic rats following treatment with highly active antiretroviral therapy (HAART) regimen triplavar. Materials and Methods: Adult male Sprague-Dawley rats (n=48) were divided into 7 groups (A-G).Treatment groups (B-G) had 7 animals per group and control group (Group A) had 6 animals per group. Diabetes was induced with streptozotocin (STZ) by intraperitoneal injection (STZ 45 mg/kg body weight). The animals were euthanized on the tenth week with kidneys removed for examination and blood obtained via cardiac puncture. Results: Key renal parameters showed no albuminuria, normal blood urea nitrogen (BUN), serum creatinine and electrolytes in all groups treated with M. charantia. Untreated diabetic (Group B) and HAART treated diabetic (Group C) showed severe albuminuria, a significantly raised BUN and serum creatinine (P<0.05) and gross electrolyte disturbances. Blood glucose levels were consistently and significantly raised in all groups not receiving the adjuvant M. charantia (P<0.05). Levels of oxidative stress enzymes Superoxide dismutase (SOD), Catalase and activities of Reduced Gluthaione (GSH) and Malondiadehyde (MDA) were significantly lower in all groups not receiving M. charantia. Histopathology in untreated diabetic and HAART treated animals showed severe degenerative changes in the glomeruli and inflammatory cellular infiltration while M. charantia treated animals showed an essentially normal glomerular appearance with capillary loops and normal cytoarchitecture. Conclusion: M. charantia extract administration improved blood glucose levels, reinstates renal function, reduces body weight loss and restores hyperglycemia.
https://ijbms.mums.ac.ir/article_13880_489dcbf3850c11c6cbaba6aa973357c1.pdf
2019-11-01
1359
1367
10.22038/ijbms.2019.31848.7663
Antiretroviral therapy
Diabetic nephropathy
Histopathology
Kidney
Momordica charantia
Sprague-Dawley rats
Ugochukwu
Offor
ugochukwuoffor@yahoo.com
1
Department of Clinical Anatomy, School of Laboratory Medicine and Medical Sciences, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, South Africa
LEAD_AUTHOR
Edwin
Coleridge Stephen Naidu
naidue@ukzn.ac.za
2
Department of Clinical Anatomy, School of Laboratory Medicine and Medical Sciences, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, South Africa
AUTHOR
Oluwatosin
Olalekan Ogedengbe
215039780@stu.ukzn.ac.za
3
Department of Clinical Anatomy, School of Laboratory Medicine and Medical Sciences, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, South Africa
AUTHOR
Ayoola
Isaac Jegede
ayoolajegede@yahoo.co.uk
4
Department of Clinical Anatomy, School of Laboratory Medicine and Medical Sciences, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, South Africa
AUTHOR
Aniekan
Imo Peter
petera@ukzn.ac.za
5
Department of Clinical Anatomy, School of Laboratory Medicine and Medical Sciences, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, South Africa
AUTHOR
Okpara
Azu Onyemaechi
azu@ukzn.ac.za
6
Department of Clinical Anatomy, School of Laboratory Medicine and Medical Sciences, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, South Africa
AUTHOR
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31