HISTOLOGICAL AND BIOCHEMICAL ASSESSMENT OF LIVER FUNCTION IN DICLOFENAC-INDUCED TOXICITY AND THE PROTECTIVE EFFECTS OF VITAMIN-E

Diclofenac, a widely used non-steroidal anti-inflammatory drug (NSAID), is associated with hepatotoxicity through oxidative stress and inflammation. This study aimed to evaluate the histological and biochemical alterations in liver function following diclofenac administration and to investigate the potential protective effects of Vitamin E in a rat model. Twenty-four adult male Wistar rats were randomly divided into four groups (n=6): Control (normal saline), Diclofenac-only (50 mg/kg body weight, i.p. for 7 days), Vitamin E-only (100 mg/kg, oral), and Diclofenac + Vitamin E. At the end of the treatment period, serum biochemical parameters (ALT, AST, ALP, total bilirubin), oxidative stress markers (MDA, SOD, CAT, GSH), and liver histology were assessed. Results showed that diclofenac significantly elevated serum liver enzymes and MDA levels while depleting antioxidant enzymes compared to the control group (p < 0.05). Histological examination revealed severe hepatocellular degeneration, necrosis, and inflammatory cell infiltration in the diclofenac-only group. Co-administration of Vitamin E significantly reduced liver enzyme levels, improved antioxidant status, and ameliorated histopathological damage, restoring near-normal liver architecture. Conclusion: Vitamin E offers substantial protection against diclofenac-induced hepatotoxicity, primarily through its antioxidant properties. These findings suggest its potential as an adjunct therapy in patients on long-term diclofenac treatment.