miR-221在急性心肌梗死大鼠中表达及其作用

发布时间：2018-02-15 02:52

本文关键词： miR- 急性心肌梗死(AMI) 表达作用　出处：《中国公共卫生》2017年06期 　论文类型：期刊论文

【摘要】：目的探讨miR-221在急性心肌梗死(AMI)大鼠中的表达及其作用。方法在45只SD清洁级雄性大鼠中随机抽取35只通过冠状动脉左前降支结扎大鼠建立AMI模型,将其中建模成功的30只大鼠随机分为AMI组、对照组及抑制组,每组各10只;另抽取未建模的10只大鼠设立假手术组,采用冠状动脉左前降支穿线不结扎。其中对照组用携带绿色荧光蛋白(GFP)的慢病毒空载体miR-221阴性对照以4×10~7病毒数量进行心肌组织局部注射转染,抑制组用携带miR-221 inhibitor慢病毒以4×10~7病毒数量进行心肌组织局部注射转染,AMI组和假手术组每天给予等量生理盐水,隔日1次连续2周;记录大鼠心脏功能。采用原位末端凋亡法(TUNEL)检测心肌凋亡指数(AI),RT-PCR法检测miR-221表达,Western blot法检测Bax、Bcl-2、PI3K和p-AKT蛋白表达。结果与假手术组大鼠miR-221表达量(0.18±0.02)比较,AMI组(1.16±0.12)和对照组(1.18±0.12)大鼠的miR-221表达量均升高(均P0.01),抑制组大鼠miR-221表达量(0.30±0.03)均低于AMI组和对照组大鼠的miR-221表达量(均P0.01);与假手术组大鼠Bax(0.13±0.01)、Bcl-2(0.53±0.05)、PI3K(0.45±0.04)和p-AKT(0.87±0.09)蛋白表达量比较,AMI组和对照组大鼠的Bax蛋白表达量均上调(均P0.01),Bcl-2、PI3K和p-AKT蛋白表达量均下调(均P0.01);抑制组大鼠较AMI组和对照组大鼠Bax表达量均下调(P0.01),Bcl-2、PI3K和p-AKT蛋白表达量均上调(P0.01)。结论 miR-221在AMI大鼠心肌组织中高表达,下调miR-221表达可通过激活PI3K/AKT信号通路调控下游蛋白Bax及Bcl-2的表达抑制AMI大鼠心肌细胞凋亡。
[Abstract]:Objective to investigate the expression and role of miR-221 in acute myocardial infarction (AMI) rats. Methods 35 SD clean male rats were randomly selected to establish AMI model by left anterior descending coronary artery ligation. Among them, 30 rats were randomly divided into AMI group, control group and inhibition group with 10 rats in each group, and 10 unmodeled rats were selected to set up sham-operation group. The left anterior descending branch of coronary artery was not ligated. The control group was transfected by local injection of 4 脳 10 ~ (7) virus with a lentivirus empty vector miR-221 carrying green fluorescent protein (GFP). The inhibitory group was injected with miR-221 inhibitor lentivirus in 4 脳 10 ~ (7) virus number by local injection of myocardial tissue into AMI group and sham-operation group. The rats in the control group were given the same amount of normal saline once a day for 2 weeks every other day. Cardiac function of rats was recorded. Myocardial apoptosis index was detected by Tunel) and miR-221 expression was detected by RT-PCR. Western blot assay was used to detect the expression of Baxan Bcl-2PI3K and p-AKT protein. Results compared with sham operation group, the expression of miR-221 was 1.16 卤0.12 in AMI group and 1.16 卤0.12 in control group. The expression of miR-221 in rats was significantly higher than that in AMI group and control group (P < 0.01). The expression of miR-221 in AMI group and control group was significantly lower than that in AMI group and control group (all P 0.01), and the expression of Bax protein in Bax(0.13 卤0.01 + Bcl-20.53 卤0.055-PI3KU 0.45 卤0.04 and p-AKT _ 3 + 0.87 卤0.09 in sham operation group was higher than that in sham operation group (P < 0.01), and the expression of p-AKT was 0.87 卤0.09 in control group and in control group (P < 0.01). The expression of P0.01Bcl-2PI3K and p-AKT were down-regulated (all P0.01A), and the expression of Bax was down-regulated in the inhibitory group than in the AMI group and the control group. Conclusion the expression of miR-221 in the myocardium of AMI rats is higher than that of the control group. Conclusion the expression of miR-221 in the myocardium of the AMI rats is higher than that of the control group, and the expression of P0.01Bcl-2pI3K and p-AKT protein is up-regulated in the myocardium of the AMI rats. Down-regulation of miR-221 expression can inhibit cardiomyocyte apoptosis in AMI rats by activating PI3K/AKT signaling pathway to regulate the expression of downstream proteins Bax and Bcl-2.
【作者单位】：牡丹江医学院第二附属医院心血管内科;
【分类号】：R542.22

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