GP IIb/IIIa是血小板聚集的最终共同受体，替罗非班作为GP IIb/IIIa阻断剂具有起效快作用强的特点，在临床上广泛使用。然而临床上存在替罗非班抵抗现象，且机制尚未完全阐明。血小板无细胞核，不存在转录水平调控，但存在miRNA介导的转录后调控。我们前期发现，miR-150-5p能降解GP IIb/IIIa的mRNA，并且在脑梗死患者中表达低，其表达与 Dicer酶正相关。我们认为，受Dicer酶调控，miR-150-5p介导的GP IIb/IIIa表达和血小板聚集，可能是替罗非班抵抗的重要原因。本研究将综合运用miR-150-5p细胞转染和基因敲除等实验技术，在细胞、动物及临床样本水平研究Dicer酶对miR-150-5p的调控，以及miR-150-5p调控GP IIb/IIIa表达和血小板聚集的机制，并开展脑梗死大鼠miR-150-5p干预研究，为替罗非班抵抗的防治提供新思路。

Platelet membrane receptor (glycoprotein IIb/IIIa, GP IIb/IIIa) is the ultimate co-receptor of platelet aggregation pathway. Tirofiban, as a GP IIb/IIIa blocker, is widely used in the treatment of cardiovascular and cerebrovascular diseases because of its rapid and strong effect. However, the phenomenon of tirofiban resistance exists in clinical practice and the mechanism has not been fully elucidated. There is no transcriptional regulation in the platelet for no nuclear, but there is miRNA mediated posttranscriptional regulation. We found that miR-150-5p can degradate the mRNA of GP IIb/IIIa, and there was low expression in patients with cerebral infarction. The expression of miR-150-5p was positively correlated with the Dicer enzyme. Therefore，we think that the high expression of GP IIb/IIIa and platelet aggregation mediated by miR-150-5p may be the important reasons of tirofiban resistance. In this study, the regulation of miR-150-5p by Dicer enzyme, the mechanism of GP IIb/IIIa expression and platelet aggregation regulated by miR-150-5p, and miR-150-5p’s intervention will be systematically studied at cellular, rat animal and clinical sample levels via in-vitro and in-vivo experimental techniques such as miR-150-5p Cell Transfection and Gene Knockout, etc. This study will provide a new idea for the prevention and treatment of tirofiban resistance.