Abstract: OBJECTIVE To explore the role of PKC-mediated ERK1/2 signaling pathway in ozone(O₃)preconditioning rat liver ischemia-reperfusion. METHODS Sixty rats were randomly divided into 6 groups:control group, ischemia reperfusion group, O₃ pretreatment group, O₃ pretreatment+ERK inhibitor group(O₃+PD98059 group), O₃ pretreatment+PKC inhibitor group(O₃+CHE group), ischemia reperfusion+PKC activator group(IR+PMA group). Except for control group, all other groups underwent liver ischemia reperfusion surgery. The O₃-related group was pretreated with O₃, and the regulator group was given the corresponding regulator. The levels of alanine aminotransferase and aspartate aminotransferase in serum of each group were detected respectively, and pathological observation was performed. Western blotting was used to detect heat shock protein 70(HSP70), protein kinase C(PKC) and extracellular regulated protein kinase 1/2(ERK1/2) expression levels in liver tissue. RESULTS Compared with the control group, ischemia reperfusion group had significantly increased liver tissue cell damage(P<0.05), and the PKC and ERK1/2 phosphorylation and HSP70 expression levels in the liver tissue were significantly increased(P<0.05). Compared with the ischemia reperfusion group, the liver tissue cells of the O₃-related group were significantly reduced(P<0.05), the phosphorylation of PKC and ERK1/2 and the expression level of HSP70 in the liver tissue were significantly increased(P<0.05). Compared with the O₃ pretreatment group, when PKC and ERK1/2 inhibitors were used, liver tissue cell damage was significantly increased(P<0.05), PKC and ERK1/2 phosphorylation and HSP70 expression levels in liver tissue were significantly reduced(P<0.05). CONCLUSION O₃ oxidative pretreatment can significantly increase the expression level of HSP70 by activating the PKC-mediated ERK1/2 signaling pathway, and significantly reduce the liver ischemia-reperfusion injury in rats.