The Protective Effect of Curcumin Against Gentamicin-Induced Renal Dysfunction and Oxidative Stress in Male Albino Rats

Abstract

Background: Generation of free radicals in the renal cortex plays an important role in the pathogenesis of gentamicin-induced nephrotoxicity. Curcumin, the yellow curry pigment isolated from turmeric, has been confirmed to have a strong antioxidant and free radical scavenging actions. In the present study, we investigated the possible protective effect of curcumin against gentamicin-induced nephropathy in male albino rats. Methods: Thirty two male albino rats were divided into 4 equal groups (Gr.): (Gr.I) control, injected i.p with 1cc isotonic saline solution/day for 8 wks; (Gr.II) received 200 mg/kg/day curcumin (Cur. ) orally, suspended in normal saline, for 8 wks ; (Gr.III) injected I.p by 100 mg/kg/day gentamicin (Gen.) for 8 days followed by 1cc saline I.p thereafter; (Gr.IV) (Cur./Gen.) received 200 mg/kg/day Cur. for one week before starting Gen injection (100 mg/kg/day) for 8 days during which Cur. was received concurrently with Gen then Cur administration was continued thereafter throughout the rest of the study (6 wks). Body weight was recorded weekly. Renal function was evaluated by measuring the 24 h. urine output, the concentrations of plasma creatinine, blood urea nitrogen (BUN) and creatinine clearance. Also, kidney weight and the parameters of oxidative stress: reduced glutathione (GSH), thiobarbituric acid reacting substance (TBARS) and the activities of superoxide dismutase (SOD), catalase and glutathione peroxidase (GPX) were measured in kidney tissue. Results: The Kidney weight, plasma creatinine, BUN and 24 h urine output were significantly increased while the body weight and creatinine clearance were significantly decreased (P < 0.0005), in rats treated with Gen. as compared to control. While Cur. could significantly normalize the previous parameters. In addition Gen. caused oxidative stress in kidney as seen by significant increase in TBARS level, and significant decrease of catalase, GSH, SOD and GPX activities (P < 0.0005), However, Cur. could normalize all the above parameters as compared to control. Conclusion: Our data indicate that Cur. could suppress renal toxicity by blocking oxidative injury in the kidney and restore the antioxidant enzymatic profile. The renoprotective effect of Cur. is also evident by a remarkable improvement of renal function in Gen. injected rats. So Cur. can be used as a potent protective agent against renal oxidative damage mediated by Gen.