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Cisplatin induced nephrotoxicity may limit the clinical use of this drug. The aim of this study was to investigate the mechanism of the possible renoprotective effect of curcumin in cisplatin nephrotoxicity. Methods: Thirty male Wistar rats were randomly divided into five groups: 1- control (0.5ml normal saline ip, daily for 10 constitutive days); 2- cisplatin (10mg/kg ip, single dose at the first day); 3- cisplatin + curcumin (10mg/kg ip, dissolved in 5% DMSO, daily for 10 constitutive days); 4- cisplatin + vehicle (5% DMSO, 0.3ml ip) and 5- curcumin (10mg/kg ip). At the end of the study, urine and blood samples were obtained for biochemical (BUN, creatinine, sodium and potassium) analysis. The right kidneys were kept in 10% formalin for H&amp;E and TUNEL staining, and the left kidneys were used for type 2 organic cation transporter (OCT2) and type 3 glutathione peroxidase (GPx3) gene expression and malondialdehyde measurements. Results: Cisplatin significantly increased serum creatinine, BUN, potassium and kidney lipid peroxidation. However, the effect of cisplatin on Gpx3 and OCT2 gene expression was not statistically significant. Curcumin treatment decreased serum creatinine, BUN, and kidney lipid peroxidation, but increased GPx3 and OCT2 gene expression. Moreover, curcumin significantly reversed the cisplatin-induced kidney tissue injury and decreased apoptosis. Conclusion: It is concluded that the ameliorative effect of curcumin in cisplatin nephrotoxicity was assumed to be due to antioxidant effect of this agent. The role of curcumin in mediating uptake of cisplatin is still unclear.

physiology and pharmacology

Possible role of glutathione peroxidase-3 and organic cation transporter-2 gene expressions in mediating protective effects of curcumin on cisplatin‐induced nephrotoxicity in rats