OBJECTIVE： To elucidate the efficacy and mechanism of Hugan tablets in hepatoprotective effects from perspective of metabolic pathways. METHODS： 36 male rats were randomly divided into normal group （0.5％sodium carboxymethyl cellulose）， model group （0.5％sodium carboxymethyl cellulose） and Hugan tablets group （1.7 g/kg）， 12 in each group， intragastrically administrated once a day， for 9 d. After 1 h of last administration， rats in model group and Hugan tablets group were intraperitoneally injected 50％CCl4 peanut oil solution 1 mL/kg to induce liver injury. After 24 h of modeling， malondialdehyde （MDA）， superoxide dismutase （SOD）， glutathione peroxidase （GSH-Px） levels in liver tissue of rats were detected. Nuclear magnetic resonance spectroscopy （1H-NMR） metabolomics technique was adopted to establish the serum and liver metabolite profiles of rats， and the effects of Hugan tablets on changes of metabolic profile and potential biomarkers in serum and liver of rats with CCl4-induced acute liver injury were analyzed. RESULTS： Compared with normal group， MDA level in liver tissue of rats in model group was significantly increased （P＜0.05）， SOD and GSH-Px levels were significantly reduced （P＜0.05）. Both body physiology and material metabolism of rats were obviously changed， and levels of 11 metabolic potential biomarkers in serum and 14 metabolic potential biomarkers in liver were significantly increased/decreased （P＜0.05）. Compared with model group， MDA level in liver tissue in Hugan tablets group was significantly reduced （P＜0.05）， SOD and GSH-Px levels were significantly increased （P＜0.05）. Serum and liver metabolism tended to be normal， 6 metabolic potential biomarkers （isoleucine， leucine， 3-hydroxybutyrate， acetone， acetoacetate， choline） in serum and 8 metabolic potential biomarkers （3-hydroxybutyrate， alanine， glutamate， pyruvate， succinate， choline， lactate， glucose） in liver got significant callback （P＜0.05）. CONCLUSIONS： The hepatoprotective mechanism of Hugan tablets may be associated with antioxidative stress and regulation of lipid metabolism， glucose metabolism and amino acid metabolism.