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Tushar Sawant* and Kedar Prabhavalkar


Introduction: Cisplatin is associated with serious adverse events which overshadowed its efficacy. Baicalin found to reduce the cisplatin-induced cytotoxicity and renal damage in animal models. The aim of the current study is to demonstrate protective effect of baicalin in cisplatin-induced toxicity models in mice. Methods: Healthy Swiss Albino mice (weight range of 20-30 g), after acclimatization divided into 8 groups (n=8): normal control, vehicle control, baicalin (50 mg/kg), cisplatin (7 mg/kg), quercetin (50 mg/kg) + cisplatin, baicalin (40, 80, and 120 mg/kg) + cisplatin. For induction of cisplatin toxicity model, cisplatin (7 mg/kg) was administered from day 11 to 15 of study period. Baicalin was administered at 40, 80, and 120 mg/kg for 15 days. On 16th day, blood samples were collected and mice were sacrificed to excise kidneys and livers. Results: In cisplatin treated group, blood urea nitrogen, creatinine, serum glutamic pyruvic transaminase, and serum glutamic-oxaloacetic transaminase levels were significantly (P<0.001) elevated compared to control group, while, baicalin showed significant (P<0.01, P<0.001, P<0.05, P<0.001 respectively) dose dependent amelioration. On histopathology, cisplatin induced pathological changes in both liver and kindney were ameliorated by baicalin cisplatin. Similarly, Tumor necrosis factor alpha, interleukin 6, and nuclear factor erythroid 2–related factor 2 levels were attenuated significantly (P<0.001) by baicalin. Conclusion: The present cisplatin-induced toxicity model indicates that baicalin may establish as a promising approach for the prevention of cisplatin-induced toxicity.

Keywords: Baicalin; cisplatin; cisplatin-induced toxicity; nuclear factor erythroid 2– related factor 2; tumor necrosis factor alpha.

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