Mitochondria-mediated mitigatory role of curcumin in cisplatin-induced nephrotoxicity

作者：Waseem Mohammad; Kaushik Pooja; Parvez Suhel^*

来源：Cell Biochemistry and Function, 2013, 31(8): 678-684.

DOI：10.1002/cbf.2955

• curcumin
• cisplatin
• oxidative stress
• mitochondria
• nephrotoxicity
• biomarkers

Cisplatin (CP) is one of the most potent chemotherapeutic anti-tumour drugs, and it has been implicated in renal toxicity. Oxidative stress has been proven to be involved in CP-induced toxicity including nephrotoxicity. However, there is paucity of literature involving role of mitochondria in mediating CP-induced renal toxicity, and its underlying mechanism remains unclear. Therefore, the present study was undertaken to examine the antioxidant potential of curcumin (CMN; a natural polyphenolic compound) against the mitochondrial toxicity of CP in kidneys of male rats. Acute toxicity was induced by a single intra-peritoneal injection of CP (6mgkg(-1)). We studied the ameliorative effect of CMN pre-treatment (200mgkg(-1)) on the toxicity of CP in rat kidney mitochondria. CP caused a significant elevation in the mitochondrial lipid peroxidation (LPO) levels and protein carbonyl (PC) content. Pre-treatment of rat with CMN significantly replenished the mitochondrial LPO levels and PC content. It also restored the CP-induced modulatory effects on altered enzymatic and non-enzymatic antioxidants in kidney mitochondria. We hypothesize that the reno-protective effects of CMN may be related to its predisposition to scavenge free radicals, and upregulate antioxidant machinery in kidney mitochondria.

• 出版日期2013-12