Diclofenac-Induced Alterations in Renal Antioxidants and Cytokines in Male Wistar Rats
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Abstract
Introduction: Diclofenac is a nonsteroidal anti-inflammatory drug (NSAID) that is widely used to treat pain and inflammation. However, diclofenac use has been associated with a number of side effects, including renal toxicity. The mechanisms underlying diclofenac-induced nephrotoxicity are not fully understood, but oxidative stress and inflammation are thought to play a role. This study investigated the effects of diclofenac on renal antioxidants and cytokines in male Wistar rats.
Method: Male Wistar rats were randomly divided into three groups: control group, low and high-dose diclofenac group (10 and 30 mg/kg/day) respectively. Treatment was administered for 10 days. At the end of the study, the rats were sacrificed, serum samples and kidney homogenates were analysed for markers of oxidative stress, lipid peroxidation and inflammation including assessment of renal function.
Result: Diclofenac treatment caused a significant decrease in renal antioxidants, including superoxide dismutase (SOD) and glutathione peroxidase (GPx) compared to the control, (0.78±0.11 versus 0.61±0.14), (214.80±46.37versus 149.70±39.43) P <0.05 respectively.
In addition, a significant increase in the level of MDA and renal cytokine (TNF-α) was observed between the control and treated group of rats (2.62±0.29 versus 8.74±4.34, p<0.001) and (1276.0±90.18 versus 222.90±38, P=<0.00) and respectively. The high-dose diclofenac caused a significant increase between the treated and control group of rats respectively and deranged renal function test (serum creatinine and renal KIM-1)
Conclusion: This study provides evidence that diclofenac may induce alterations in renal antioxidants, and mediates oxidative stress and inflammation with consequent kidney injury in male Wistar rats.
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References
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