OBJECTIVE： To study the improvement effect and related mechanism of pyragrel sodium on nerve function of cerebral ischemia-reperfusion injury model rats. METHODS： Totally 72 SD rats were randomly divided into sham operation group， model group， positive control group （dizocilpine 0.8 mg/kg）， pyragrel sodium low-dose， medium-dose and high-dose groups （20， 30， 45 mg/kg）， with 12 rats in each group. Except sham operation group received sham operation， rats in the other groups were treated with middle cerebral artery ligation to induce cerebral ischemia-reperfusion injury model. The rats in the sham operation group and the model group were injected with the constant volume of normal saline， for consecutive 6 d， and the interval of administration was 24 hours. After 24 h reperfusion and last medication， neurological deficit score and postural reflex score in rats were evaluated. The situation of cerebral injury （including whole brain， insular cortex， putamen， striatum， somatic cortex， amygdala， motor cortex） was evaluated by using micropositron emission tomography. The rats were sacrificed， and the situation of cerebral infarction was observed by TTC and cerebral infarction volume was calculated. Na+-K+-ATPase， Ca2+-ATPase activity and Glu content were detected by ELISA. RESULTS： Compared with sham operation group， neurological deficit score and postural reflex score increased significantly in model group 24 h after ischemia-reperfusion and after last medication （P＜0.05 or P＜0.01）. After 24 hours of cerebral ischemia-reperfusion and the last medication， SUV of brain tissue， SUV ratio of right left brain of different cerebral areas were decreased significantly （P＜0.01）. After last medication， the percentage of cerebral infarction volume was increased significantly （P＜0.01）； the activities of Na+-K+-ATPase and Ca2+-ATPase were decreased significantly （P＜0.01）， while Glu content was increased significantly （P＜0.01）. Compared with model group， above indexes of pyragrel sodium low-dose， medium-dose and high-dose group， positive control group were all improved significantly （P＜0.05 or P＜0.01）. CONCLUSIONS： Pyragrel sodium can improve cerebral ischemia-reperfusion injury and nerve function， which is related to the activity up-regulation of Na+-K+-ATPase and Ca2+-ATPase， the down-regulation of Glu content.