To study the protective mechanism of breviscapine on rats with vascular endothelial cell injury and its mechanism on the Wnt/β-catenin signaling pathway.Methods:Sixty SD rats were randomly divided into a healthy group，a model group，a low-dose breviscapine group(BL group)，and a high-dose breviscapine group(BH group)，with 15 rats in each group.Blood vessel morphology was observed by HE staining，and the mRNA expression of Wnt，FZD1，AXIN1，GSK-3β，β-catenin，and VEGF was detected by RT-PCR.TNF-α and CRP were measured by ELISA.The morphology of vascular endothelial cells was observed under the microscope.MTT was used to measure vascular endothelial cell proliferation.The levels of Wnt，FZD1，AXIN1，GSK-3β，β-catenin，and VEGF were measured by Western blot.Results:There were no obvious changes in the blood vessels of healthy rats.The model rats showed obvious vascular injury.Vascular injury was improved in the BL group and the BH group，especially in the BH group.Compared with the healthy group，the model group showed wider space between vascular endothelial cells and smaller and exfoliated cells.The vascular endothelial cells of the BL group were similar to those of the model group.The BH group had narrowed vascular endothelial cell space and reduced apoptosis，and the morphology was improved.Compared with the healthy group，the model group showed decreased OD values of Wnt，VEGF，FZD1，β-catenin，AXIN1，and vascular endothelial cells at different time points，and increased apoptosis rates of GSK-3β，TNF-α，CRP，and vascular endothelial cells(P<0.05).Compared with the model group，the BL and BH groups showed increased OD values of Wnt，VEGF，FZD1，β-catenin，AXIN1，and vascular endothelial cells at different time points and decreased apoptosis rates of GSK-3β，TNF-α，CRP，and vascular endothelial cells(P<0.05)，and such changes were more significant in the BH group(P<0.05).Conclusion:Breviscapine can control vascular stability by regulating the expression of the Wnt/β-catenin pathway，thereby protecting against vascular endothelial cell injury in rats.