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Curcumin ameliorates diclofenac sodium-induced nephrotoxicity in male albino rats
Ahmady Y Ahmed1, Amany M Gad1, Ola M Abd El-Raouf1
1Department of Pharmacology, National Organization for Drug Control and Research, NODCAR, Giza, Egypt.
Abstract:
Exposure to drugs often results in toxicity in the kidney which represents the major control system maintaining homeostasis of the body and thus is especially susceptible to xenobiotics. Nephrotoxicity is a life-threatening side-effect of nonsteroidal anti-inflammatory drugs (NSAIDs). Diclofenac is one of the most frequently prescribed NSAIDs and have been reported to cause multiple organs damage. Curcumin (CUR) exhibits nephroprotective properties. Therefore, rats were divided into four groups; rats of groups 3 and 4 received diclofenac (100 mg/kg, i.m.), whereas rats of groups 2 and 4 received CUR (100 mg/kg, p.o.) for 3 days. Diclofenac revealed a significant increase in urea and creatinine levels and malondialdehyde concentration and marked reduction in catalase activity and reduced glutathione concentration. Histopathologically, diclofenac produced fatty changes and eosinophilic casts were detected in the renal tubules, those were attenuated by administration of CUR prior diclofenac.
Insights
This study shows that diclofenac causes kidney damage in rats, evidenced by altered biochemical markers and kidney tissue changes. Curcumin treatment effectively protected against diclofenac-induced nephrotoxicity.
Area of Science:
- Pharmacology
- Toxicology
- Nephrology
Background:
- Kidney toxicity (nephrotoxicity) is a serious risk associated with nonsteroidal anti-inflammatory drugs (NSAIDs).
- Diclofenac, a common NSAID, can damage multiple organs, including the kidneys.
- Curcumin (CUR) has demonstrated potential kidney-protective effects.
Purpose of the Study:
- To investigate the nephroprotective effects of curcumin against diclofenac-induced kidney toxicity in a rat model.
Main Methods:
- Rats were administered diclofenac (100 mg/kg) and/or curcumin (100 mg/kg) orally or intramuscularly for 3 days.
- Evaluated kidney function through urea and creatinine levels.
- Assessed oxidative stress markers, including malondialdehyde, catalase activity, and reduced glutathione.
- Conducted histopathological examination of renal tissues.
Main Results:
- Diclofenac administration significantly increased urea and creatinine levels, elevated malondialdehyde, and decreased catalase activity and reduced glutathione.
- Histopathology revealed fatty changes and eosinophilic casts in renal tubules following diclofenac exposure.
- Curcumin treatment prior to diclofenac administration attenuated these adverse effects.
Conclusions:
- Diclofenac induces significant nephrotoxicity in rats, characterized by impaired kidney function and oxidative stress.
- Curcumin exhibits notable nephroprotective properties, mitigating diclofenac-induced kidney damage.
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