Hepatoprotective effects of a polyherbal extract (PHE) containing Averrhoa carambola and Lepidium sativum with trigonelline against CCl4-induced hepatotoxicity in Wistar rats

Background: This study was designed to evaluate the hepatoprotective potential of a polyherbal extract (PHE) containing Averrhoa carambola, Lepidium sativum, and trigonelline against carbon tetrachloride (CCl₄)-induced liver injury in Wistar rats. Although individual components possess known antioxidant and hepatoprotective properties, comprehensive pharmacological evaluation of their combined use remains limited. This study aimed to investigate possible synergistic effects on liver function, oxidative stress, and hepatic tissue morphology. Methodology: Seven groups of Wistar rats (n = 6 per group) were administered PHE orally at doses of 400 and 600 mg/kg body weight for 21 consecutive days. On day 22, hepatotoxicity was induced using CCl4. Hepatoprotective activity was assessed by measuring serum liver biomarkers, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total bilirubin. Oxidative stress parameters, including superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and lipid peroxidation (LPO), were also evaluated. Histopathological examination of liver tissues was performed. Result and Discussion: PHE significantly reduced serum ALT, AST, ALP, and bilirubin levels by 55–65% compared to the toxic control group. Lipid peroxidation decreased by approximately 60%, while antioxidant enzymes SOD and CAT increased by over 70%, demonstrating marked attenuation of oxidative stress. Histopathological analysis revealed substantial preservation of hepatic architecture, comparable to that observed with the standard drug silymarin. Conclusion: The strong antioxidant and hepatoprotective properties of PHE suggest its potential as a holistic alternative to conventional therapies for liver damage. Its ability to restore liver function and structure highlights its effectiveness against chemically induced hepatocyte injury.