Objective：To explore the effect of sevoflurane postconditioning on renal ischemia/reperfusion injury，and to determine whether its protective mechanism is related to the anti-inflammation and anti-oxidation. Methods：Male C57BL/6 mice were randomly and equally divided into four groups：sham operation group（Sham group），sham operation+ sevoflurane postconditioning group（Sham+Sevo group），renal ischemia/reperfusion injury group（IR group）and renal ischemia/reperfusion injury + sevoflurane postconditioning group（Sevo-Post C group）. The renal ischemia/reperfusion injury model was induced by left renal pedicle clamping for 30 min followed by 24 h reperfusion and right nephrectomy. The mice were inhaled 2% sevoflurane for 1 h at the start of reperfusion in Sevo-Post C group. After 24 h reperfusion，renal functional parameters，serum mediator concentrations and markers of oxidative stress in kidney tissues were determined，and renal histopathological analysis was performed. The protein including p-Akt，p-GSK3β，Akt and GSK3β were determined by Western blot. Results：Serum creatinine（Scr），blood urea nitrogen（BUN），TNF-α，IL-6，and MDA concentrations were significantly increased after renal I/R as compared with the sham group（P＜0.05）. Sevoflurane postconditioning reduced Scr，BUN，TNF-α，IL-6，and MDA levels（P＜0.05），and decreased histological scores（P＜0.05）. The phosphorylation levels of renal Akt and GSK3β were elevated after renal ischemia/reperfusion injury，and sevoflurane postconditioning further increased the phosphorylation levels of them as compared with the IR group（P＜0.05）. Conclusion：Sevoflurane postconditioning protected against renal IR injury possibly through the anti-inflammatory and antioxidative effects induced by the activation of Akt/ GSK3β signialing pathway.