Irbesartan Attenuates Gentamicin-induced Nephrotoxicity in Rats through Modulation of Oxidative Stress and Endogenous Antioxidant Capacity

BACKGROUND: Overproduction of reactive oxygen species and free radicals is the main mechanism beyond gentamicin-induced nephrotoxicity. Irbesartan and other angiotensin II blockers offer significant nephroprotective effect through improvement of renal function and reduction of renal inflammation. Therefore, the objective of this study was to illustrate the nephroprotective effect of irbesartan in rats regarding the oxidative stress of irbesartan biomarkers. METHODS: Thirty male Sprague–Dawley rats were used; they were divided into three groups: Group I (10 rats) treated with distilled water, Group II (10 rats) treated with gentamicin, and Group III (10 rats) treated with gentamicin plus irbesartan for 12 days. Blood urea, serum creatinine, serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione reductase (GSH), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule (KIM-1), and cystatin-c were measured in each group. RESULTS: Irbesartan significantly reduced blood urea, serum creatinine, serum MDA, NGAL, KIM-1, and cystatin-c [P < 0.05]. Irbesartan significantly increases SOD [P < 0.05] without significant effect in elevation of GSH serum levels. CONCLUSIONS: This study concluded that irbesartan has a nephroprotective effect in attenuation of acute nephrotoxicity through modulation of oxidative stress and antioxidant capacity in rats.