The long-term heavy consumption of alcohol results in the development of alcohol-related liver disease, which is the second leading cause of death among all liver diseases(1–2). Oxidative stress is considered as one of the key mechanisms responsible for alcoholic liver damage(3–4). In the present study, the protective effects of 5% ethanol extract (SME) from Salvia miltorrhiza Bunge. against alcoholic liver damage were investigated in male C57BL/6 mice. Mice (n 9 per group), which received SME (100 or 400 mg/kg b.w./d) with ethanol revealed complete prevention of alcohol-induced hepatotoxicity as evidenced by the significant reductions of serum aspartate aminotransferase and alanine aminotransferase activities, compared with ethanol-alone administered mice (5 g ethanol/kg b.w./d). When compared with the ethanol-alone treated group, the mice receiving ethanol plus SME exhibited significant increases in hepatic antioxidant activities, including superoxide dismutase, catalase, glutathione-S-transferase, glutathione peroxidase, glutathione reductase and glutathione. Furthermore, the amelioration of malondialdehyde levels indicated SME's protective effects against liver damage mediated by alcohol in vivo. Also, the pre-treatment with SME significantly suppressed ethanol-induced increase in the expression of cytochrome P-450 2E1 (CYP2E1), a major contributor in generating a state of oxidative stress, which results in hepatotoxicity(5). These results suggest that 5% ethanol extract of S. miltorrhiza Bunge. has protective action against alcohol-induced toxicity in the liver by suppressing the expression of CYP2E1 and recovering the antioxidant status.