缺血再灌注损伤中miR-126的作用及对心肌细胞凋亡的影响

郎明健; 王越; 李志; 陈娇; 何培根

doi:10.13406/j.cnki.cyxb.001365

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缺血再灌注损伤中miR-126的作用及对心肌细胞凋亡的影响

基础研究 | 更新时间：2024-01-17

- 缺血再灌注损伤中miR-126的作用及对心肌细胞凋亡的影响
- Role of miR-126 in myocardial ischemia reperfusion injury and its influence on myocardial cell apoptosis
- 重庆医科大学学报 2017年42卷第9期页码：1131-1136
- 作者机构：
  
  湖北医药学院附属东风医院心血管内科
- 作者简介：
- 基金信息：
  
  湖北省自然科学基金重点资助项目(编号:2060402-791)
- DOI：10.13406/j.cnki.cyxb.001365
  中图分类号： R54
- 纸质出版日期：2017，
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郎明健, 王越, 李志, 等. 缺血再灌注损伤中miR-126的作用及对心肌细胞凋亡的影响[J]. 重庆医科大学学报, 2017,42(9):1131-1136.

Lang Mingjian, Wang Yue, Li Zhi, et al. Role of miR-126 in myocardial ischemia reperfusion injury and its influence on myocardial cell apoptosis[J]. Journal of Chongqing Medical University, 2017,42(9):1131-1136.
郎明健, 王越, 李志, 等. 缺血再灌注损伤中miR-126的作用及对心肌细胞凋亡的影响[J]. 重庆医科大学学报, 2017,42(9):1131-1136. DOI： 10.13406/j.cnki.cyxb.001365.

Lang Mingjian, Wang Yue, Li Zhi, et al. Role of miR-126 in myocardial ischemia reperfusion injury and its influence on myocardial cell apoptosis[J]. Journal of Chongqing Medical University, 2017,42(9):1131-1136. DOI： 10.13406/j.cnki.cyxb.001365.

摘要

目的:通过体内外实验探讨微小RNA(miR)-126在心肌缺血再灌注损伤中的作用及机制。方法:体外部分:心肌细胞H9C2分6组

建立心肌细胞模拟缺血/再灌注(simulated ischemia/reperfusion

SI/R)损伤模型

并分别转染miR-126mimic和miR-126inhibitor。qRT-PCR检测心肌细胞miR-126表达

流式细胞术检测细胞凋亡

Western blot检测caspase-3及其裂解片段的蛋白表达。体内部分:雌性Wistar健康大鼠分5组

建立缺血/再灌注损伤(ischemia/reperfusion

I/R)模型

并分别转染含有GFP的空病毒、miR-126mimic以及miR-126inhibitor的慢病毒。测定各组大鼠心肌梗死范围

TUNEL测定心肌细胞凋亡。结果:与对照组相比

心肌细胞H9C2SI/R后miR-126表达(0.32±0.02)明显降低(P=0.000)、细胞凋亡率(3.8±0.6)明显上升(P=0.000);与SI/R相比

采用miR-126mimic上调miR-126表达后细胞凋亡率(5.3±0.8)明显增加(P=0.007)

caspase-3表达(0.450±0.003)明显降低(P=0.000)

而采用miR-126inhibitor下调miR-126表达后细胞凋亡率(2.9±0.5)明显降低(P=0.000)

caspase-3表达(1.80±0.03)明显升高(P=0.002)。与假手术组相比

I/R组和I/R+GFP组心肌梗死范围[(59.4±2.5)

(60.2±2.8)]明显增加(P=0.000

P=0.000)

而与I/R组相比

I/R+miR-126mimic组心肌梗死范围(69.0±2.4)明显增加(P=0.013)

而I/R+miR-126inhibitor组心肌梗死范围(39.5±2.5)明显降低(P=0.000);TUNEL检测结果显示

与假手术组相比

I/R组和I/R+GFP组心肌细胞凋亡率[(33.4±1.7)

(33.7±1.8)]明显升高(P=0.000

P=0.000);而与I/R组相比

I/R+miR-126mimic组心肌细胞凋亡率(42.2±2.3)明显增加(P=0.003)

而I/R+miR-126inhibitor组心肌细胞凋亡率(25.5±1.5)明显降低(P=0.000)。结论:心肌缺血再灌注损伤会引起miR-126表达降低

而上调miR-126表达会促进心肌细胞凋亡

相反抑制miR-126表达可能有助于预防心肌缺血再灌注引起的心肌细胞凋亡。

Abstract

Objective:To explore the mechanism of miR-126 in myocardial ischemia reperfusion injury. Methods:In vitro

myocardial cells H9C2 were divided into 6 groups

and the myocardial cell simulated ischemia/reperfusion（SI/R）injury model was established

transfecting with the miR-126 mimic and miR-126 inhibitor. The expression of miR-126 was detected with real time-PCR in myocardial cells;apoptosis was detected with flow cytometry;and the expression of caspase-3 and its fragmentation were detected with Western blot. In vivo

healthy female Wistar rats were divided into 5 groups

and ischemia/reperfusion injury model was established.They were respectively disposed with the transfection of empty GFP

miR-126 mimic and miR-126 inhibitor virus. Myocardial infarction range was detected and the myocardial cell apoptosis was detected with TUNEL. Results:Compared with those of control group

the expression of miR-126 in myocardial cell H9C2 after SI/R was significantly reduced and the rate of apoptosis increased significantly. Up-regulation of miR-126 expression by miR-126 mimic could raise apoptosis rate and reduce caspase-3 expression significantly. On the contrary

down-regulation miR-126 expression by miR-126 inhibitor could reduce apoptosis rate and raise caspase-3 expression significantly. Compared with that of control group

myocardial infarction range increased significantly in the I/R group and the I/R +GFP group. Compared with that of I/R group

myocardial infarction range in the I/R+miR-126 mimic group reduced significantly. TUNEL test results showed that compared with that of control group

the myocardial cell apoptosis rate in I/R group and the I/R+GFP group increased significantly. Compared with that of I/R group

the myocardial cell apoptosis rate in I/R+miR-126 mimic group increased significantly

while myocardial cell apoptosis rate in the I/R + miR-126 inhibitor group decreased significantly

with statistically significant differences（P<0.05）.Conclusion:miR-126 is down-regulated in myocardial ischemia-reperfusion injury and that the promotion of miR-126 may promote myocardial cell apoptosis

while the inhibition of miR-126 may protect against myocardial cell apoptosis caused by ischemia-reperfusion.

关键词

miR-126心肌缺血再灌注损伤实验研究

Keywords

miR-126ischemia reperfusion injuryExperimental study

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