Preclinical Protective Activity of Lutein on Diclofenac-induced Hepatotoxicity

Background: Diclofenac (DF), a non-steroidal anti-inflammatory drug, may cause hepatotoxicity. Lutein (LT), a naturally occurring compound, has potential therapeutic activities. The protective activity of LT against DF-induced hepatotoxicity in adult Wistar rats was evaluated in this study. Methods: Twenty adult Wistar rats weighing 240-250 g of both sexes were randomized into 4 groups of n=5/group. The rats were given the chemical agents intraperitoneally for 7 days as follows: Group 1 (control) and Group 2 were given sterile water (1 mL/kg/day) and LT (40 mg/kg/day), respectively. Group 3 was given DF (10 mg/kg/day), while Group 4 was supplemented with LT (40 mg/kg/day) prior to the administration of DF (10 mg/kg/day). On day 8, the rats were weighed, euthanized, and blood samples were collected and evaluated for serum biochemical markers. The liver tissues of the rats were weighed and assessed for histological changes and oxidative stress markers. Results: DF decreased body weight and increased liver weight significantly at p<0.01 when compared to the control. DF elevated serum lactate dehydrogenase, alkaline phosphatase, gamma glutamyl transferase, conjugated bilirubin, aminotransferases, total bilirubin, and liver malondialdehyde levels significantly at p<0.001 when compared to the control. Liver glutathione, catalase, superoxide dismutase, and glutathione peroxidase levels were significantly (p<0.001) decreased by DF when compared to the control. DF caused hepatocyte necrosis. However, LT supplementation abrogated DF-induced changes in all evaluated parameters significantly at p<0.001. LT supplementation restored liver histology. Conclusion: LT shows potential therapeutic benefit against DF-induced hepatotoxicity.