慢性炎症反应和炎细胞不断穿经内皮细胞进入内膜是动脉粥样硬化发生的关键环节。纤维蛋白β链的N端Bβ15-42为VE-cadherin的绑定配体，纤维蛋白通过与内皮细胞间的VE-cadherin结合，诱导结合在纤维蛋白Aα17-19的炎细胞向内膜下迁移，而与β链N端序列相匹配的Bβ15-42模拟肽能竞争性阻断炎细胞迁移。现已证实纤维蛋白Bβ15-42/VE-cadherin途径参与了动脉粥样硬化炎症进程，但具体作用机制尚不明确。因此本课题通过建立高表达VE-cadherin的人内皮细胞-单核细胞共培养体系和兔动脉粥样硬化模型，应用合成的Bβ15-42模拟肽和我国自主研发的蚓激酶主要组分A（EFEa）对该途径进行干预，从离体和在体水平研究Bβ15-42/VE-cadherin途径在动脉粥样硬化炎症进程中的作用，以及特异性拮抗该途径后对动脉粥样硬化转归的影响，为抗动脉粥样硬治疗提供新的思路和靶点。

The key event in the development/process of Atherosclerosis (AS) is chronic inflammation reaction and inflammatory cells continuously travelling into vascular intima via/through endothelial cells. The N-terminal Bβ15-42 of fibrin β chain is the binding ligands of VE-cadherin of endothelial cells. Fibrin induced inflammatory cells that combined with fibrin Aα17-19 to migrate to subendothelial layer by binding to VE-cadherin, and the mimetic peptide which matched the sequences of the N-terminal of fibrin β can block inflammtory cells migration competitively. It has been proved fibrin Bβ15-42/ VE-cadherin pathway invoved in the inflammatory process of AS, but the underlying mechanism was unclear. In the study, we set up/created/established Human endothelial cells and mononuclear cells co-cultured system and an atherosclerotic model of rabbit which expressed VE-cadherin in high level. Based on these models, we applied the synthetic mimetic peptide of Bβ15-42 and the major ingredient A (EFEa) of lumbrokinase which was developed by our country to intervene Bβ15-42/ VE-cadherin pathway and observed its role in the inflammatory process of AS both in vitro and in vivo models. In addition, we explored the effect of the specific antagonism against Bβ15-42/ VE-cadherin pathway on the outcome of AS. Thereout, we will provide some new ideas and targets for anti- atherosclerosis according to/by the stduy.