Objective：To discuss whether salidroside(Sal)can protect the injured neurons in rats after cerebral ischemiareperfusion through regulating the activity of janus kinase 2/signal transducer and activator of transcription 3(JAK2/STAT3)signaling pathway.Methods：A total of 30 healthy adult male SD rats were randomly divided into the sham operation group，the model group and the Sal group，10 rats in each group.In the model group and the Sal group，the rat models with middle cerebral artery occlusion(MCAO)were established by Longa's suture-occluded method.The Sal group was given 50 mg/kg of Sal solution by intraperitoneal injection after occlusion for two hours，and the model group and the sham operation group with no middle cerebral artery occlusion received intraperitoneal injection of saline of the same volume at the same time.All groups were given administration once a day for six days.The score of injury of nerve function in each group was recorded.The apoptosis in brain tissue in each group was detected by TUNEL method；the expression of JAK2，p-JAK2，STAT3 and p-STAT3 protein by Western blot method；and the expression of mRNA of B-cell lymphoma-2(Bcl-2)by RP-qPCR.Results：Compared with those in the sham operation group，the score of injury of nerve function in the model group was increased(P＜ 0.05)，the number of apoptotic neurocytes in the brain tissue was significantly increased(P＜ 0.05)，and the expression of p-JAK2 and p-STAT3 protein and mRNA of Bcl-2 was significantly increased(P＜0.05).Compared with those in the model group，the score of injury of nerve function in the Sal group was decreased(P ＜ 0.05)，the number of apoptotic neurocytes in the brain tissue was significantly decreased(P＜ 0.05)，and the expression of p-JAK2 and p-STAT3 protein and mRNA of Bcl-2 was significantly decreased(P＜0.05).Conclusion：Sal can significantly improve the injury of nerve function in rats after cerebral ischemia-reperfusion and reduce neuronal apoptosis in the brain tissue，whose mechanism may be the regulation of the activity of JAK2/STAT3 signaling pathway.