缺血再灌注（I/R）可引起自噬和凋亡导致心肌细胞损伤，我们前期研究发现，I/R损伤的内皮细胞，在异丙酚刺激时能够释放具有心肌保护作用的微囊泡（propofol-EMVs），但机制不明。随后我们采用RNA sequence测序发现Propofol-EMVs内lnc-CCT4-1明显升高，而生物信息学分析发现lnc-CCT4-1其中一个靶基因eIF4B为凋亡相关基因，这些提示lnc-CCT4-1可能通过eIF4B参与异丙酚保护心肌IR损伤的过程。所以本项目拟采用RNA sequence、基因转染、WB等细胞和分子生物学技术，通过体内外观察Propofol-EMVs携带lnc-CCT4-1对凋亡关键基因eIF4B靶向调控及心肌细胞凋亡的影响，阐明Propofol-EMVs通过lnc-CCT4-1靶向eIF4B抑制细胞凋亡的新机制，为临床有效防治I/R提供新策略新方法。

Ischemia/reperfusion (I/R) can lead to myocardium cell injury induced by autophagy and apoptosis. Although the mechanism is remained unknown, our previous study observed the cardio-protective effect of endothelial derived microvesicles induced by propofol (Propofol-EMVs) in I/R stress. RNA sequencing showed that lnc-CCT4-1 was significantly increased in propofol-treated EMVs. Meanwhile, Bioinformatics analysis revealed that one of the target genes of lnc-CCT4-1, eIF4B, was an apoptosis-related gene indicating that lnc-CCT4-1 may be involved in the protective effect of propofol on myocardial I/R injury through eIF4B. With RNA sequencing, Gene transfection, Western blotting and other cell and molecular biological techniques, this project intends to observe the targeted regulating effect of Propofol-EMVs-carrying lnc-CCT4-1 on eIF4B in myocardial apoptosis and further reveal the corresponding mechnism, providing a new strategy for the clinical prevention and treatment of I/R.