Objective: To investigate the mechanism of Radix Kansui (RK) stir-fried with vinegar (VRK)decreased hepatotoxicity in mice.Methods: According to a random number table,40 mice were randomly divided into negative control group (0.5％ carboxymethylcellulose sodium,20 mL/kg),positive control group (0.1％ mixture of carbon tetrachloride in soybean oil,20 mL/kg),RK group (the ethyl acetate extracts of RK,250 g crude drug/kg) and VRK group (the ethyl acetate extracts of VRK,250 g crude drug/kg) with 10 mice per group.All mice were administered orally by gavage daily for 7 continuous days.The morphology of liver tissues was examined to assess the liver injury by a transmission electron microscope.Hepatocyte apoptosis in vivo was determined by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nickend labeling (TUNEL) assay.Immunohistochemical technique was adopted to detect the expression of particular antiapoptotic and proapoptotic proteins in the mitochondrial pathways,including B-cell lymphoma (Bcl-2) and caspase-3,as well as the expression of inflammatory mediators,including nuclear factor kappa B (NF-κ B) and intercellular adhesion molecule-1 (ICAM-1).Results: Liver injury and hepatocyte apoptosis were observed in RK mice,and the liver injury were significantly reduced in VRK-treated mice.In immunohistochemistry study,compared with the negative control group,RK inhibited dramatically the Bcl-2 protein expression and significantly increased the expression of caspase-3,NF-κ B and ICAM-1 (all P＜0.01).Compared with the RK group,VRK group induced significant increase on Bcl-2 protein expression,and decreased the caspase-3,NF-κ B and ICAM-1 protein expression (P＜0.05 or P＜0.01).Conclusion: The mechanism of reduced hepatotoxicity of VRK may be associated with the reduced inflammation,regulation of antiapoptotic and proapoptotic mediators in the mitochondrial pathway.