Oxidative damage and inflammation are implicated in the pathogenesis of liver injury and fibrosis. In the present study, we investigated the molecular mechanism by which gomisin A conferred a hepatoprotective effect, focusing on its antioxidant and anti-inflammatory effects using rats with carbon tetrachloride (CCl 4 )-induced acute liver injury. Pretreatment with gomisin A prior to the administration of CCl 4 markedly prevented an increase in alanine aminotransferase, aspartate aminotransferase, and histological hepatic lesions. Gomisin A was also associated with a decrease in hepatic lipid peroxidation, and increased superoxide dismutase activity, suggesting that gomisin A has an antioxidant effect. In addition gomisin A treatment ameliorated mRNA levels of CCl 4 -induced inflammatory mediators, including tumor necrosis factor-α, interleukin-1β and inducible nitric oxide (NO) synthase, and the protein levels of transcriptional upregulator nuclear factor kappa B (NF-κB) and phospho-inhibitor of NF-κB (IκB). Furthermore, α-smooth muscle actin (α-SMA), a myofibroblast marker, was also inhibited by gomisin A treatment. These results suggest that gomisin A inhibits the oxidative stress and activation of NF-κB, leading to down-regulation of pro-inflammatory mediators and amelioration of fibrogenesis.Key words gomisin A; oxidative stress; inflammatory response; carbon tetrachloride; acute liver injuryThe liver has the important function of metabolizing and eliminating biological and xenobiotic compounds. Liver injury is considered to be a serious health problem leading to acute hepatitis, cholestasis, and cirrhosis. Hepatocellular injury usually leads to oxidative stress, inflammation, and activation of the innate immune system. These factors lead to the release of pro-inflammatory cytokines (that can result in hepatic necrosis) and of pro-fibrogenic cytokines that may cause increased synthesis of extracellular matrix components by activation of quiescent hepatic stellate cells (HSCs).