Abstract: Glial scar formation is a reactive cellular process mainly involving heavy proliferation of reactive astrocytes that occurs after cerebral ischemia reperfusion injury.Notably，glial scar has been proven to have detrimental effects in neuroregeneration.One hand，the glial scar prevents axonal extensions via physical and chemical approaches，on the other hand，many neuro-developmental inhibitor molecules are secreted by the reactive astrocytes within the scar that prevent complete functional recovery of the central nervous system after cerebral ischemia reperfusion injury.Endocannabinoids involve in the regulation of the proliferation of reactive astrocytes.To explore the effect of synthetic cannabinoid receptor agonist WIN55，212-2 on glial scar formation after cerebral ischemia reperfusion injury，a middle cerebral artery occlusion (MCAO) model in adult rats was used in this study.The expression of Vimentin (markers for activated astrocytes)，GFAP (markers for astrocytes)，Neurocan (markers for chondroitin sulfate proteoglycan-3)，and Jagged-1(ligands for Notch-1 signaling pathway) were determinated by immunofluorescence staining.To determine potential drug target for WIN55，212-2，a specific inhibitor of cannabinoid receptor 1-rimonabant combine WIN55，212-2 treatment was also studied.The results showed that WIN55，212-2 significantly inhibited the glial scar formation through decreasing the reactive astrocytes proliferation，and the Jagged-1 expression in the reactive astrocytes via cannabinoid receptor 1.