Abstract: The aim of this research was to observe the expression of ACE2 on injury liver which induced by CCl4, and its mechanism of antiinjury. 16 SD rats was randomly divided into two groups: control group and experiment group. The rats in control group were injected strokephysiological saline solution and the experiment group were injected 40% CCl4, respectively. The first dosage was 5 mL·kg-1, then 3 mL·kg-1 every three days. Four weeks later, the activities of ALT, AST and the concentrations of albumin, total protein , total bilirubin and AngⅡwere detected. We also analyzed the distribution and expression of ACE2 and Mas on liver by Realtime PCR and hybridization in situ. Compared with control group, the average daily weight gain, the concentration of albumin and total protein were markedly reduced (P<0.05), but the activities of ALT and AST were obviously increased (P<0.05).The concentrations of TBIL and AngⅡ had no significantly different compared with control group. The mRNA expression levels of ACE2 and Mas receptor were increased(3.21±0.52 vs 1.03±0.11, P<0.01;1.64±0.22 vs 1.02±0.10, P<0.05). The distribution of ACE2 was widespread throughout cirrhotic nodules, bile duct cells and endothelial cells lining small blood vessels. The expression of ACE2 and Mas receptor on injury induced by CCl4 in rats were increased significantly, which suggested that ACE2 may play an important role on injury liver by activating the ACE2Ang 17Mas axis to rival the effect of AngⅡ which could evoke injury.