Pharmacotherapeutic potentials of astragalin against cisplatin-induced renal toxicity via regulating Nrf-2/keap-1 pathway

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Purpose Cisplatin (CP) is a chemotherapeutic drug that can produce toxic effects in many organs of the body including kidney. Thus, the current trial was executed for 30 days to assess the alleviative effects of AST to avert CP instigated renal injuries. Materials and methods Forty-eight male albino rats were allocated into four groups including control, CP (10 mg/kg), CP+AST (10 mg/kg + 50mg/kg) and only AST (50 mg/kg). On the completion of trial, the rats were dissected and further analyses were performed. Results CP intoxication increased the expressions of pro-apoptotic markers (Caspase-3 and Bax) while reducing the expressions of Nrf-2 and antiapoptotic marker (Bcl-2) and lowering the expressions and activities of antioxidant enzymes i.e., GPx, GSR, CAT, HO-1, GST, SOD and GSH contents. Furthermore, CP intoxication elevated the levels of oxidative stress markers (MDA and ROS) and inflammatory markers (IL-6, IL-1 β, TNF-α, NF-kB and COX-2). CP exposure also disrupted the levels of renal function markers and renal histology. However, AST treatment ameliorated all the renal alterations induced by CP-exposure. Conclusion Therefore, AST protected the renal tissues from CP-instigated damages due to its antioxidant and reno-protective potential.