We investigated the hepatoprotective potential of Ferula communis extract for CCI4 induced liver damage. We used six groups of rats: group 1, untreated control; group 2, CCl4 treated (hepatotoxic); group 3, treated with 150 mg/kg F. communis; group 4, treated with 300 mg/kg F. communis; group 5, treated with CCl4 + 150 mg/kg F. communis; and group 6, treated with CCl4 + 300 mg/kg F. communis. Liver damage was produced by injection of 1 ml/kg CCI4 twice/week. Extracts of F. communis, 150 and 300 mg/kg/day, were administered for 8 weeks. The effects of F. communis were assessed by measuring aspartate aminotransferase (AST), alanine aminotransferase (ALT), γ-glutamyl transferase (GGT) and total bilirubin (T-BIL) levels, and the activities of antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GPx) in the liver. The histology and immunohistochemistry of liver tissue were evaluated using hematoxylin and eosin staining, and caspase 3 and 8-OHdG immunostaining. F. communis extract produced significant reductions in elevated levels of ALT, AST, GGT and T-BIL and increased levels of GPx and SOD in rats treated with CCl4. F. communis extract decreased CCl4 induced 8-OHdG formation and caspase 3 activation significantly in hepatocytes, especially at the 150 mg/kg dose. Our findings demonstrate the potential efficacy of F. communis for attenuating CCl4 induced hepatotoxicity and oxidative damage.