Thalidomide Ameliorates Cisplatin-Induced Nephrotoxicity by Inhibiting Renal Inflammation in an Experimental Model

摘要: Cisplatin is a platinum-based chemotherapy drug. However, its chemotherapeutic use restricted by serious side effects, especially nephrotoxicity. Inflammatory mechanisms have significant role in the pathogenesis of cisplatin-induced Thalidomide an immunomodulatory and anti-inflammatory agent used for treatment various inflammatory diseases. The purpose this study was to investigate potential nephroprotective effect thalidomide mouse model Nephrotoxicity induced mice single injection cisplatin (15 mg/kg, i.p.) treated with (50 100 mg/kg/day, orally) 4 days, beginning 24 h prior injection. Renal toxicity demonstrated increasing plasma levels creatinine blood urea nitrogen (BUN). increased renal production proinflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, transforming growth (TGF)-β1. In addition, kidney malondialdehyde (MDA), myeloperoxidase (MPO), nitric oxide (NO) were cisplatin. Biochemical results showed that reduced increase BUN. also significantly tissue cytokines, MDA, MPO, NO cytokine IL-10. Furthermore, histological examination indicated ameliorated damage caused These data suggest attenuates nephrotoxicity possibly inhibition reactions. Taken together, our findings indicate might be valuable candidate prevention patients receiving