Effects of butein against cisplatin-induced nephrotoxicity and oxidative stress in mice

Abstract

Nephrotoxicity is one of the life-threatening side effects of cisplatin when used in the treatment of a wide variety of both pediatric and adult malignancies. Accumulating evidence suggests that cisplatin treatment induces oxidative stress and reduces antioxidant status leading to apoptosis of renal cells. The purpose of this study was aimed to explore the effect of butein, a potent antioxidant, against cisplatin induced nephrotoxicity in mice. Single intraperitoneal administration of dose of cisplatin (20 mg/kg) caused marked renal damage, characterized by a significant increase in serum creatinine and blood urea nitrogen (BUN). Cisplatin also increased relative weight of kidney with higher kidney lipid peroxidation levels, and lowered kidney superoxide dismutase (SOD) and catalase (CAT) activities. Histological examinations revealed renal tubular degeneration, extensive epithelial vacuolization and a large number of infiltrated inflammatory cells in cisplatin alone treated mice. The results showed that treatment with butein attenuated cisplatin induced kidney injury and significantly inhibited serum creatinine and BUN levels and restored antioxidant enzyme activities in kidney tissue. Histological studies exhibited that butein treatment reduced tubular degeneration, and epithelial vacuolization with reduce infiltrated inflammatory cells in kidney. The present study demonstrates that butein can effectively suppress cisplatin induced nephrotoxicity by inhibiting oxidative stress.