Ｏｂｊｅｃｔｉｖｅ　To investigate the effect of sevoflurane postconditioning on extracellular signaling-regulated kinase（ERK）1/2 after cerebral ischemia/reperfusion injury（I/RI） in rats.　Methods　Rat middle cerebral artery occlusion（MCAO） model was bulit. Seventy male Sprague-Dawley（SD） rats were randomly assigned to 7 groups （with 10 rats each）： Sham group， I/RI group， sevoflurane postconditioning group（Sevo group）， U0126/PD98059 ［specific inhibitor of mitogen-activated protein kinase（MAPK）/ERK1/2］ group， Sevo+U0126 group and Sevo+PD group. All rats except the Sham group were subjected to 90 min of MCAO followed by 24 h reperfusion. Sevoflurane was administrated at the beginning of reperfusion for 30 min. U0126/PD98059 was given by intracerebroventricular injection 30 min before ischemia. The neurological deficit scores and infarct volume were evaluated at the end of reperfusion. Total ERK1/2 and Phosphrylated-ERK1/2（ERK1/2 P42/P44） were measured by Western blot analysis.　Results　Compared with the Sham group， both of the neurological deficit scores and infarct volume increased in I/RI group and Sevo group（P＜0.05）. Compared with I/RI group， significantly decreased neurological deficit scores and infarct volume［（3.2±0.6） vs （2.2±0.4） and （42.3±2.2）% vs （24.1±2.1）%， respective］（P＜0.05）， significantly increased ERK1/2 P42/P44 expression were found in the Sevo group（P＜0.05）. There was no significant difference in all variables among U0126 group， PD group， Sevo+U0126 group and Sevo+PD group（P＞0.05）.　Conclusions　Sevoflurane postcondnioning may protect brain I/RI in rat perhaps contribute to activation of the ERK1/2 signaling pathway.