Cisplatin-induced nephrotoxicity is related to an increase in lipid peroxidation and oxygen free radicals in kidney. Acetylsalicylic acid (ASA) has been suggested to be an antioxidant besides its well known therapeutic effects and is also known to improve lipid profile via acting as a free radical scavenger. This study aimed to investigate the possible protective effects of ASA on the extent of renal damage in cisplatin-induced nephrotoxicity. A total of 40 rats were divided into four equal groups. The first group was served as vehicle control, the second group (ASA group) was treated with 100 mg/ kg bw, orally, for 5 days, the third group (cisplatin group) was received cisplatin only 7mg/kg bw, i.p., single dose, while the fourth group (ASA + cisplatin group) was administered ASA 100 mg/kg bw, orally for 5 days and cisplatin 7mg/kg bw, i.p., single dose on day 2 of the experiment. Cisplatin administration induced a marked nephrotoxicity as evidenced by a significant decrease in creatinine clearance with severe reduction of renal blood flow and a significant increase in blood urea, serum creatinine and urine volume compared with the control rats. In addition, histopathological assessment revealed marked tubular necrosis, degeneration, tubular dilatation and luminal cast formation. Cisplatin also induced oxidative stress as indicated by significant increase in kidney tissue concentrations of malondialdehyde (MDA) and significant decrease in glutathione (GSH) content of renal tissues. ASA supplementation produced significant increase in creatinine clearance and renal blood flow with significant decrease in blood urea, serum creatinine and urine volume. ASA treatment caused a significant reduction of the elevated renal MDA level and a significant increase in the GSH content of kidney tissues. Furthermore, ASA ameliorated cisplatin-induced pathological changes in kidneys when compared to cisplatin group alone. In conclusion, ASA significantly protected against cisplatin-induced nephrotoxicity and oxidative stress in rat through its antioxidant properties but not enough to inhibit renal dysfunction completely. |
