OBJECTIVE： To study the effects of tilianin（TIL） on brain tissue in rats with cerebral ischemia-reperfusion injury. METHODS： Totally 120 male SD rats were randomly divided into sham operation group （0.9％ sodium chloride solution）， model group （0.9％ sodium chloride solution）， nimodipine group （32 mg/kg） and TIL low-dose and medium-dose， high-dose groups （4， 8， 16 mg/kg）， with 20 rats in each group. The rats were given relevant medicine intragastrically， once a day， for consecutive 7 d. 15 min after last medication， cerebral ischemia-reperfusion injury model was established by reforming suture-occluded method. The neurological deficit score in rats were evaluated， and percentage of cerebral infarction volume of rats was determined. Histopathological changes of brain tissue were observed by HE staining. The activities of SOD， CAT and LDH， MDA content in cerebral tissue of rats were determined. The expression of calcitonin gene-related peptide （CGRP） and peripheral vascular endothelial growth factor receptor 2 （VEGFR2） protein were determined by Western blot assay. RESULTS： Compared with sham operation group， neurological deficit score and percentage of cerebral infarction volume of model group were increased significantly （P＜0.01）； the nerve cells in brain tissue were significantly reduced and the interstitial edema was obvious. SOD and CAT activities were decreased significantly， LDH activity was increased significantly， MDA content was decreased significantly，protein expression of CGRP and VEGFR2 were increased significantly （P＜0.05 or P＜0.01）. Compared with model group， neurological deficit score of nimodipine group， TIL medium-dose and high-dose groups were decreased significantly； percentage of cerebral infarction volume was decreased significantly （P＜0.05 or P＜0.01）； above pathological conditions of cerebral tissue in rats were relieved significantly； SOD and CAT activities were strengthened significantly， MDA content and LDH activities were decreased significantly， protein expression of CGRP and VEGFR2 were increased significantly （P＜0.05 or P＜0.01）. CONCLUSIONS： TIL has certain protective effects on cerebral ischemia-reperfusion injury model rats， and its mechanism may be related to the up-regulation of CGRP and VEGFR2 expression.