基础医学与临床 ›› 2021, Vol. 41 ›› Issue (12): 1786-1791.

• 研究论文 • 上一篇    下一篇

抑制miR-155对心肌缺血/再灌注模型心肌细胞凋亡及炎性反应的影响

朱新华, 刘蓓蓓, 侯静雯, 李秋影, 许慧娟, 张晓阳*   

  1. 新疆医科大学第五附属医院 老年病科, 新疆 乌鲁木齐 830000
  • 收稿日期:2021-01-11 修回日期:2021-05-06 发布日期:2021-12-03
  • 通讯作者: *47143185@qq.com

Effect of inhibiting miR-155 on apoptosis and inflammation reaction in myocardial ischemia-reperfusion model

ZHU Xin-hua, LIU Bei-bei, HOU Jing-wen, LI Qiu-ying, XU Hui-juan, ZHANG Xiao-yang*   

  1. Department of Geriatrics, the Fifth Affiliated Hospital of Xinjiang Medical University, Urumqi 830000, China
  • Received:2021-01-11 Revised:2021-05-06 Published:2021-12-03
  • Contact: *47143185@qq.com

摘要: 目的 探讨抑制miR-155对心肌缺血/再灌注(MI/R)模型心肌细胞凋亡及炎性反应的影响。方法 以大鼠心肌细胞系H9c2为研究对象,将细胞分为4组:空白对照组、心肌缺血再灌注组(MI/R组)、阴性对照组、miR-155 抑制剂组。RT-qPCR检测各组心肌细胞miR-155、NF-κB信号通路相关基因和Bax、Bcl-2 mRNA表达水平;ELISA检测IL-8、TNF-α的含量;流式细胞测量术检测心肌细胞凋亡率;Western blot检测各组细胞NF-κB信号通路相关基因和Bax、Bcl-2蛋白表达。结果 与空白对照组相比,MI/R组miR-155表达水平均显著升高(P<0.05);与MI/R组相比,miR-155抑制剂组miR-155表达水平显著降低(P<0.05)。MI/R组心肌细胞凋亡率、IL-8、TNF-α的含量、Bax及NF-κB信号通路相关基因蛋白及mRNA表达水平均较空白对照组显著升高,而Bcl-2蛋白和mRNA表达水平降低(P<0.05);抑制miR-155表达后,心肌细胞凋亡率、IL-8、TNF-α的含量、Bax及NF-κB信号通路相关基因蛋白及mRNA表达水平均显著降低,而Bcl-2蛋白和mRNA表达水平升高(P<0.05)。结论 抑制miR-155表达可通过降低细胞凋亡及炎性反应,从而对MI/R损伤起保护作用,其可能的作用机制是抑制NF-κB信号通路的活化。

关键词: miR-155, 心肌缺血/再灌注, 凋亡, 炎性反应, NF-κB信号通路

Abstract: Objective To explore the effect of inhibiting miR-155 on cardiomyocyte apoptosis and inflammation in myocardial ischemia-reperfusion (MI/R) model. Methods Myocardial cells of H9c2 rats were divided into four groups: blank control group, myocardial ischemia-reperfusion group (MI/R group), negative control group and miR-155 inhibitor group. The expressions of miR-155, NF-κB signaling pathway related genes and Bax, Bcl-2 mRNA were detected by RT-qPCR. The contents of IL-8 and TNF-α were detected by ELISA. Western blot was used to detect the expression of NF-κB signaling pathway related genes and Bax, Bcl-2 protein. Results Compared with the control group, the expression of miR-155 in MI/R group was significantly increased (P<0.05) while the expression of miR-155 in miR-155 inhibitor group was significantly decreased (P<0.05). In MI/R group, the apoptosis rate, the content of IL-8 and TNF-α, the protein and mRNA expression of Bax and NF-κB signal pathway were significantly higher than those in the control group, while the protein and mRNA expression of Bcl-2 were lower (P<0.05). After inhibition the expression of miR-155, the apoptosis rate, the content of IL-8 and TNF-α, the protein and mRNA expression level of Bax and NF-κB signal pathway related gene were significantly decreased, while the protein and mRNA expression by Bcl-2 were increased (P<0.05). Conclusions Inhibition of miR-155 expression can protect MI/R injury through inhibition of apoptosis and inflammation. The potential mechanism is the inhibition of the activation of NF-κB signaling pathway.

Key words: miR-155, myocardial ischemia-reperfusion, apoptosis, inflammatory, NF-κB signaling pathway

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