急性动脉血栓形成是心肌梗死、脑梗死的病理学基础，而血小板聚集在动脉血栓形成中起核心作用。因此，抗血小板聚集成为治疗缺血性心脑血管疾病的基石。目前的抗血小板药物都是抑制循环系统中全部血小板的功能，导致出血风险增加，临床净获益遇到了“天花板”。选择性抑制微血栓部位的血小板聚集有望在抑制血栓扩展的同时，不影响远隔部位的血小板生理性止血功能。本研究拟探讨经特殊短肽修饰的脂质体包被抗血小板药物对于血小板血栓部位血小板的靶向抑制作用，从而阻止急性血栓性事件发生。我们首先合成CREKA短肽、AGDV短肽和GPLGIAGQ短肽修饰的包被抗血小板药物替格瑞洛的脂质体（PMLT），然后探索MMP-2酶促药物释放条件，PMLT的体外生物安全性、抑制血小板聚集的效应、靶向结合并抑制血小板血栓的作用，进而进行动物实验研究PMLT体内生物安全性、稳定性，最后利用动物血栓模型证明PMLT可以选择性地抑制血小板血栓形成。

Acute arterial thrombosis is the pathological basis of myocardial infarction and cerebral infarction, and platelet aggregation plays an important role in arterial thrombosis. Therefore, anti-platelet aggregation is the cornerstone of the treatment of ischemic cardiovascular and cerebrovascular diseases. Current antiplatelet drugs inhibit the function of all platelets in the circulatory system, resulting in an increased risk of bleeding and a "ceiling" of net clinical benefits. Selective inhibition of platelet aggregation at microthrombus sites is expected to inhibit the expansion of thrombus without affecting the physiological hemostasis of platelets at distant sites. The aim of this study is to investigate the targeting inhibitory effect of antiplatelet drugs coated with liposomes modified by special short peptides on platelet thrombosis sites, so as to prevent the occurrence of acute thrombotic events. We will firstly synthesized CREKA peptide, AGDV peptide and GPLGIAGQ peptide modified liposomes (PMLT) encapsulating antiplatelet drug tigrello. Then we will explore the conditions of MMP-2 enzymatic drug release, the biological safety of PMLT in vitro, the effect of inhibiting platelet aggregation, targeting binding and inhibiting platelet thrombosis. Then we conduct animal experiments to study the biological safety and stability of PMLT in vivo. Finally, animal thrombosis model is used to show that PMLT could selectively inhibit platelet thrombosis. We expect to lay a foundation for clinical precise antiplatelet therapy.