کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2540703 | 1122604 | 2014 | 7 صفحه PDF | دانلود رایگان |
• The effect of etoricoxib on oxidative injury induced with (I/R) in rat kidney
• The kidneys underwent biochemical and immunohistochemical analyses.
• Etoricoxib reduced levels of MDA, MPO, COX-2, and it prevented loss of tGSH, SOD and CAT.
• Etoricoxib decreased caspase-3 gene expression and increased Bcl-2 gene expression in a dose-dependent manner.
• Etoricoxib can be used in the prevention of I/R injury in a clinical setting.
The purpose of this study was to investigate the effect of etoricoxib on oxidative injury induced with ischemia–reperfusion (I/R) in rat kidney tissue in terms of biochemistry and immunohistochemistry.Male Albino Wistar rats were divided into renal I/R (RIR), 50 mg/kg etoricoxib + RIR (ETO-50), 100 mg/kg etoricoxib + RIR (ETO-100) and sham operation (SG) groups. Animals in the ETO-50 and ETO-100 groups were given etoricoxib by the oral route at dosages of 50 and 100 mg/kg, respectively. The RIR and SG groups were given distilled water as solvent. One hour after drug administration, 1 h of ischemia and 3 h of reperfusion were applied to the left kidneys of all rats (apart from SG) under 25 mg/kg thiopental sodium anesthesia. At the end of that time, kidneys were extracted and biochemical and immunohistochemical analyses were performed.Etoricoxib reduced, in a dose-dependent manner, levels of MDA, MPO and COX-2 that normally rise with I/R in rat kidney tissues. Etorixicob did not alter COX-1 activity at 50 and 100 mg/kg doses, but significantly prevented loss of tGSH in tissues with I/R. In addition, Bcl-2′ gene expression inhibited with I/R was prevented in renal tubular and glomerular cells. Furthermore, etoricoxib significantly decreased the caspase-3 gene expression which increased with I/R.Etoricoxib significantly prevented I/R injury in a dose-dependent manner. The results of this study show that etoricoxib treatment could decrease kidney injury during IR.
Journal: International Immunopharmacology - Volume 23, Issue 1, November 2014, Pages 179–185