微小RNA-34a调控高糖诱导H9c2心肌细胞凋亡的初步研究

被引：8

作者：

赵芳

汪瀚

陈明

周斌

卫银芝

干学东

熊世熙

王扬凎

机构：

[1] 武汉大学中南医院心血管内科

来源：

中华老年心脑血管病杂志 | 2013年 / 15卷 / 11期

关键词：

微RNAs; 糖尿病; 肌细胞,心脏; 细胞凋亡; 聚合酶链反应; 基因,bcl-2;

D O I：

暂无

中图分类号：

R541 [心脏疾病];

学科分类号：

1002 ; 100201 ;

摘要：

目的探讨微小RNA-34a(miR-34a)对高糖诱导的H9c2心肌细胞凋亡的影响。方法将培养的H9c2心肌细胞随机分为3组:正常组(葡萄糖浓度5.5mmol/L)、高糖组(葡萄糖浓度33mmol/L),抑制剂组(miR-34a抑制剂浓度50nmol/L+葡萄糖33mmol/L)。采用定量PCR检测miR-34a和凋亡相关基因Bcl-2基因表达的变化,Western blot检测凋亡相关蛋白Bcl-2表达的变化;采用流式细胞术检测细胞凋亡。结果与正常组比较,高糖组心肌H9c2细胞凋亡率明显升高(P<0.05),H9c2细胞miR-34a表达显著上调(P<0.05),H9c2细胞Bcl-2mRNA和蛋白表达减少(P<0.05)。与高糖组比较,抑制剂组H9c2细胞凋亡明显下降(P<0.05),H9c2细胞Bcl-2mRNA和蛋白表达明显升高(P<0.05)。结论 miR-34a能调控高糖所致的H9c2心肌细胞凋亡,可能是通过直接抑制抗凋亡基因Bcl-2的表达而实现的。

引用

页码：1184 / 1188

页数：5

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