LAUSR

Objectives: Cisplatin is well-known for its wide chemotherapeutic effects but has limited clinical use due to its nephrotoxicity which may lead to cardiac dysfunction or failure. Galangin (3, 5, 7-trihydroxyflavone) extracted from the rhizome of Galangal is documented to possess anti-inflammatory and anti-oxidant properties. Hence, we evaluate the effect of galangin in cisplatin-induced nephrotoxicity in the model of rats Methods: Male Wistar rats were divided into six groups (n = 6 in each group) as normal, galangin (25, 50 and 100 mg/kg per oral), cisplatin-control and per se (100 mg/kg per oral). Total dosing period was ten days. On the 7th day, 8 mg/kg intraperitoneal cisplatin was administered to all groups except normal and per se group. Rat hearts were punctured followed by blood collection for evaluation of biochemical parameters. Also, kidneys were isolated for ultrastructural, immunohistochemical and histopathological studies. Results: Cisplatin increased oxidative stress and inflammation along with impairment of renal function. It also decreased the expression of the anti-apoptotic protein Bcl-2 and increased expression of pro-apoptotic proteins Bax and caspase-3. The renal tubular damage was evident in ultrastructural and immunohistochemical studies. A 100 mg/kg per oral dose of Galangin preserved renal function, morphology, suppressed oxidative stress, inflammation and the activation of apoptotic pathways. TUNEL assay documented a decrease in DNA fragmentation with galangin pre-treatment. Galangin (100 mg/kg) pre-treatment had shown to reduce the expression of NF&kgr;B along with other proteins. Conclusion: Galangin remediates cisplatin-induced nephrotoxicity thereby contributing to normal renal function.