Pathological and Ameliorative Effect of Curcumin Against Toxic Effect of Diclofenac Sodium In The Rabbits

Abstract

Background: Diclofenac sodium is a commonly prescribed non-steroidal anti-inflammatory drug (NSAID), valued for its analgesic and anti-inflammatory efficacy. However, its long-term or excessive use has been associated with adverse organ effects, most notably hepatotoxicity, likely mediated through oxidative stress and inflammatory pathways. Curcumin, a natural polyphenolic compound isolated from Curcuma longa, has attracted growing scientific interest for its antioxidant, anti-inflammatory, and hepatoprotective properties, positioning it as a promising candidate for mitigating drug-induced tissue injury.
Aim: The present study was designed to assess the gross and histopathological alterations induced by diclofenac sodium administration and to evaluate the potential protective role of curcumin against diclofenac-induced toxicity in a rabbit model.
Results: Twenty healthy rabbits were randomly divide into four equal groups: control group, diclofenac-treated group, curcumin-treated group, and diclofenac plus curcumin-treated groups. Diclofenac sodium was administered as a single intramuscular dose of 10 mg/kg.bw, while curcumin extract was administered orally at 50 mg/kg daily for five consecutive days beginning on the day of diclofenac administration. Clinical observations and gross pathological examinations of the liver, kidneys, and spleen were performed at the end of the experiment. Diclofenac administration induced marked gross hepatic lesions, including necrosis, hyperemia, and swelling, whereas no obvious pathological alterations were observed in the kidneys or spleen. Curcumin alone produced no detectable lesions, while co-administration of curcumin with diclofenac reduced the severity of hepatic changes. The findings indicate that diclofenac sodium primarily induces hepatic damage in rabbits, while curcumin exhibits a potential protective effect against diclofenac-induced liver injury. These results support the possible use of curcumin as a natural ameliorative agent to reduce NSAID-associated hepatotoxicity.
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