Objective：To investigate the effect of peroxisome proliferator-activated receptor γ（PPARγ） activator rosiglitazone in rat hepatic ischemia-reperfusion injury and its mechanism. Methods：The model of 70% warm ischemia-reperfusion injury was established in SD rats. Rats were divided randomly into 6 groups：control group, sham group, ischemia-reperfusion group, rosiglitazone group，2-chloro-5-nitrobenzanilide（GW9662） treatment group and rosiglitazone plus GW9662 treatment group. After reperfusion, AST and ALT levels in serum were detected. The liver tissue was removed for measurement of the apoptotic index by TUNEL assay, and the expression of Bax, Bcl-2 and caspase-3 proteins in ischemic hepatocytes were detected by immunohistochemistry. Results：Compared with sham group, the apoptotic index of hepatocytes, expressions of Bax, Bcl-2 and Caspase-3 proteins in ischemia-reperfusion group and rosiglitazone group was greatly increased. Compared with ischemia-reperfusion group, the apoptosis index of hepatocytes, expressions of Bax and Caspase-3 in rosiglitazone group decreased, with Bcl-2 increased. GW9662 abolished the protective effect of rosiglitazone. GW9662 treated alone increased the apoptosis index of hepatocytes, Bax and Caspase-3, with the expression of Bcl-2 decreased. Conclusion：PPARγ activator rosiglitazone could protect against ischemia-reperfusion injury in rats，with its possible mechanism of upregulating the expression of Bcl-2, inhibiting the expression of Bax and Caspase-3, and prohibiting hepatocyte apoptosis.