Allicin modulates diclofenac sodium induced hepatonephro toxicity in rats via reducing oxidative stress and caspase 3 protein expression

Purpose: This study was designed to evaluate the protective effects of allicin against diclofenac sodium induced hepatonephro toxicity in rats. Methods: Sixty male Wister albino rats were assigned into six groups. The control group received calcium carbonate and corn starch. 2nd group received diclofenac sodium (2 mg/kg bw orally) for 30 days. 3th group received allicin (45 mg/kg bw orally) for 30 days. 4th group administrated diclofenac sodium as in the 2nd group and allicin (15 mg/kg bw orally) for 30 days. 5th group received diclofenac sodium as in the 2nd group and allicin (30 mg/kg bw orally) for 30 days. 6th group received diclofenac sodium as 2nd and allicin (45 mg/kg bw orally) for 30 days. Results: Diclofenac sodium significantly elevated activities of serum aspartate aminotransferase and alanine aminotransferase and serum levels of creatinine and urea. In addition, it induced hyperglycemia, lipid peroxidation, pathological alteration and caspase 3 protein expression in hepatic and renal tissues. However, it decreased reduced glutathione concentration and proliferating cell nuclear antigen protein expression in hepatic tissues. In contrast, allicin modulated the diclofenac sodium induced alteration in liver and kidney functions and structures dose dependently. Conclusion: This study indicated that allicin had potential preventive effects against diclofenac sodium induced hepatonephro toxicity in rats.