心肌梗死后MicroRNA-24调控心肌细胞凋亡的作用研究

摘要

Objective In mice after myocardial infarction (MicroRNA-24, miR-24) study of the effects of the expression and regulation of myocardial cell apoptosis. Method Established mouse model of myocardial infarction, using real-time quantitative polymerase chain reaction (qRT-PCR) quantitative detection of miR-24 expression after myocardial infarction in myocardial tissue;construct the lentivirus carrying miR-24 and liposome, on myocardial infarction tissues were cultured by local injection of lentiviral transfection of miR-24 and myocardial cells transfected with miR-24;measured and compared mice cardiac function and the area of myocardial infarction. Result QRT-PCR detection showed, ligation group in experiment ifrst, second week, the expression level of miR-24 in myocardial infarction area and the surrounding region in the fall, and the sham operation group, the expression level of comparative difference was signiifcant (P<0.05). Upregulation of miR-24 myocardial infarction area and the surroundingarea in the fourth week, restored to the level of sham operation group, the expression level of miR-24 between the two groups had no signiifcant difference (P>0.05);transfection of lentivirus 3 days later, using the method of qRT-PCR quantitative myocardial infarction local miR-24 expression level, results showed elevated expression the levels of myocardial transfection group mice miR-24 local miR-24, compared with the blank lentivirus transfection group difference in miR-24 expression was significant (P < 0.05); blank lentivirus transfection group and miR-24 transfected group compared with the sham operation group, LVEDD and LVESD were increased, LVEF and LVFS was decreased;level decreased after transfection of LVEDD, but the difference between the blanklentivirus transfection group and miR-24 transfected group was not signiifcant (P>0.05), LVESD after transfection, reduce differences, between the two groups was signiifcant (P<0.05), the expression level in miR-24 transfected group and blank lentivirus transfection group, LVEF and LVFS increased, the difference was signiifcant (P<0.05);differences between the 2 week blank lentivirus transfection group, miR-24 transfection group, model group of myocardial infarction area had signiifcant difference (P<0.05), after two two shows a comparison between the miR-24 transfection group and blank lentivirustransfection group area difference was signiifcant (P < 0.05). Conclusion The myocardial tissue after myocardial infarction, Micro RNA-24 lower expression, can inhibit cell apoptosis after infarction, improve myocardial function.%目的对小鼠心肌梗死后MicroRNA-24（miR-24）的表达变化及其调控心肌细胞凋亡的作用研究。方法建立小鼠心肌梗死模型，利用实时定量聚合酶链式反应（qRT-PCR）定量检测心肌梗死后心肌组织中miR-24的表达水平；构建携带miR-24的慢病毒及脂质体，对心梗组织进行局部注射慢病毒转染miR-24及心肌原代细胞转染miR-24；测量并比较小鼠心功能及心肌梗死面积的差异。结果qRT-PCR检测显示，结扎组在实验的第1、2周时心肌梗死区和周边区域中miR-24的表达水平下降，与假手术组表达水平比较差异具有显著性（P＜0.05）。第4周时心肌梗死区和周边区域中miR-24的表达水平上调，恢复到假手术组的水平，两组之间miR-24的表达水平比较差异无显著性（P＞0.05）；转染慢病毒3天后，应用qRT-PCR方法定量心肌梗死局部miR-24的表达水平，结果显示miR-24转染组小鼠心肌局部miR-24的表达水平升高，与空白慢病毒转染组心肌比较miR-24的表达水平差异具有显著性（P＜0.05）；空白慢病毒转染组和miR-24转染组与假手术组相比左室传张末期内径（LVEDD）和左室收缩末期内径（LVESD）都升高，左室射血分数（LVEF）和左室短轴缩减率（LVFS）都降低；LVEDD转染后降低，但在空白慢病毒转染组和miR-24转染组之间差异无显著性（P＞0.05）， LVESD转染后降低，两组之间差异具有显著性（P＜0.05），LVEF和LVFS在miR-24转染组高于空白慢病毒转染组，差异具有显著性（P＜0.05）；转染后2周，空白慢病毒转染组、miR-24转染组、模型组之间的心肌梗死面积差异具有显著性（P＜0.05），经两两比较显示miR-24转染组和空白慢病毒转染组之间的面积比较差异具有显著性（P＜0.05）。结论心肌梗死后心肌组织miR-24低表达，能够抑制梗死后心肌细胞的凋亡，改善心肌功能。