OBJECTIVE： To explore the protective effect and its mechanisms of Sinomenium acutum polysaccharide on mice with acute alcoholic liver injury. METHODS： 60 mice were randomly divided into blank control group （normal saline）， model group （normal saline）， bifendate group （positive control， 150 mg/kg） and S. acutum polysaccharide low-dose， medium-dose， high-dose groups （100， 200， 400 mg/kg）， 10 in each group， intragastrically administrated， once a day， for continual 7 d. 1 h after last administration， mice received 50％ ethanol （0.1 mL/10 g） intragastrically to induce acute alcoholic liver injury model except for those in blank control group. After 12 h， alanine aminotransferase （ALT）， aspartate aminotransferase （AST） levels in serum， malondialdehyde （MDA）， superoxide dismutase （SOD）， glutathione （GSH）， glutathione peroxidase （GSH-Px） levels in liver tissue of mice were determined； hematoxylin-eosin staining was conducted to observe the pathological changes in liver tissue； flow cytometry was used to detect the cell apoptosis rate. RESULTS： Compared with blank control group， mice in model group showed pathological changes in edema， disordered cell arrangement and local necrosis； ALT and AST levels in serum， MDA level in liver tissue and hepatocyte apoptotic rate were significantly increased， while the SOD， GSH and GSH-Px levels in liver tissue were significantly decreased， with statistical significances （P＜0.01）. Compared with model group， cell degeneration and necrosis degree of mice were improved in S. acutum polysaccharide medium-dose and high-dose groups； except for cell apoptosis rate of liver in S. acutum polysaccharide low-dose group was not decreased significantly， the above-mentioned indicators in other treatment groups were significantly improved （P＜0.05 or P＜0.01）. CONCLUSIONS： S. acutum polysaccharide shows obvious protective effect on mice with acute alcoholic liver injury， its mechanism might relate to anti-oxidation stress and inhibiting hepatocyte apoptosis.