The effect of etoricoxib on kidney ischemia-reperfusion injury in rats: a biochemical and immunohistochemical assessment

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2014Author
Süleyman, BahadırAlbayrak, Abdülmecit
Kurt, Nezahat
Demirci, Elif
Gündoğdu, Cemal
Aksoy, Mehmet
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Suleyman, B., Albayrak, A., Kurt, N., Demirci, E., Gundogdu, C., Aksoy, M. (2014). The effect of etoricoxib on kidney ischemia-reperfusion injury in rats: a biochemical and immunohistochemical assessment. International Immunopharmacology, 23(1), 179-185. https://doi.org/10.1016/j.intimp.2014.06.042Abstract
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, Bd-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. (C) 2014 Elsevier B.V. All rights reserved.