Oxidative stress is important in pathogenesis of liver fibrosis, which is the result of deposition of excessive ECM proteins produced by activated hepatic stellate cells (HSCs). Reducing reactive oxygen species (ROS) production decreases collagen accumulation in liver. We investigated the benefits of antioxidant therapy in liver fibrosis and its association with HSC apoptosis. Forty-five male Spraque-Dawley rats were subdivided into three groups. Group I was treated with CCl(4) plus taurine, Group II with CCl(4) plus saline, and Group III with saline for 12 weeks. Erythrocyte and liver malondialdehyde (MDA) levels, superoxide dismutase (SOD) activities, Glutathione peroxidase (GSHpx) activities, and serum and liver TIMP-1 and MMP-13 levels were measured. Histopathological examinations were performed. Activated and total HSCs were quantified immunohistochemically. Apoptotic HSCs were detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining. Taurine decreased histopathological injury scores and oxidative stress parameters significantly. The number of activated HSCs was significantly higher in taurine untreated group ( [Formula: see text] ). Serum and tissue MMP-13 levels were significantly higher and TIMP-1 levels were significantly lower in taurine-treated group ( [Formula: see text] and [Formula: see text], respectively). The number of apoptotic activated hepatic stellate cells was significantly higher with taurine treatment ( [Formula: see text] ). Preventing the production of reactive oxygen species is effective in inhibiting fibrogenesis in experimental rat model. Inhibitory activity of this agent on HSCs' activation, apoptosis, and further fibrogenic events should be clearly identified.