Abstract
Diclofenac (DIC) can cause nephrotoxicity in humans. In this study, we evaluated the protective effects of N-acetyl cysteine (NAC) on DIC-induced nephrotoxicity. Rats were assigned to four groups. Group 1 was control group; group 2 administrated with DIC only; group 3 administrated with DIC plus NAC and group 4 was treated with DIC and silymarin. Then, the oxidative biomarkers in serum and kidney were evaluated. In group 2, DIC caused a remarkable elevation (p < 0.05) in the levels of serum uric acid, TNF-α, creatinine, urea, GOT, and GPT, protein carbonyl, malondialdehyde (MDA), and renal TNF-α gene expression, relative to control group. In treated groups with NAC and silymarin, a noticeable reduction (p < 0.05) was seen in mentioned levels of biochemical parameters. NAC showed that it could reduce the abnormality of biochemical parameters and histopathological changes which is induced by DIC. PRACTICAL APPLICATIONS: N-acetyl cysteine (NAC) has a potential to ameliorate renal histopathological changes and improving renal activity of antioxidant enzymes in nephrotoxicity by diclofenac. Also, NAC has a potential to reduce inflammatory gene expression in the diclofenac-induced nephrotoxicity. Additionally, NAC can be considered as an antioxidant which reduces renal MDA and serum protein carbonyl due to nephrotoxicity by diclofenac.
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