缺糖缺氧心肌细胞中miRNA-155对Notch信号通路及自噬和凋亡的影响  

Effects of miRNA-155 on Notch signaling pathway and autophagy and apoptosis of myocardial cells in oxygen-glucose deprivation model

作　　者：陈希妍[1] 马彦娟[1] 牛丽丹[1] 杨亚琴[1] 杨飞云[1] 石金河[1] CHEN Xiyan;MA Yanjuan;NIU Lidan;YANG Yaqin;YANG Feiyun;SHI Jinhe(Department of Emergency,the First Affiliated Hospital of Xinxiang Medical University,Weihui 453100,China)

机构地区：[1]新乡医学院第一附属医院急诊科,河南卫辉453100

出　　处：《实用医学杂志》2021年第3期304-307,共4页The Journal of Practical Medicine

基　　金：国家自然科学基金青年基金(编号:81600677)。

摘　　要：目的探讨miRNA-155在缺糖缺氧心肌细胞模型中对Notch信号通路及心肌细胞凋亡与自噬的影响。方法建立缺糖缺氧细胞(oxygen-glucose deprivation,OGD)模型,细胞分为正常对照组,OGD组,OGD组+miRNA-155 inhibitor阴性对照组及OGD组+miRNA-155 inhibitor组。利用RT-qPCR检测模型组与正常对照组心肌细胞中miRNA-155的表达情况;利用Western blot检测正常对照组,OGD组,OGD组+miRNA-155抑制剂阴性对照组及OGD组+miRNA-155抑制剂组中Notch1,HES1,Beclin1及Caspase-3的表达情况;利用CCK-8实验检测各组心肌细胞的活性。结果 RT-qPCR结果显示,与正常对照组相比较,模型组心肌细胞中miRNA-155的表达显著升高;Western blot结果显示,抑制miRNA-155的表达后,可显著升高缺糖缺氧心肌细胞中Notch1,HES1,Beclin1的表达,降低细胞中Caspase-3的表达;CCK-8实验结果显示,抑制miRNA-155的表达后,可显著提高缺糖缺氧心肌细胞的活性。结论 MiRNA-155 inhibitor可通过提高Notch1及HES1的表达,促进Notch信号通路激活,促进细胞自噬,抑制细胞凋亡,提高心肌细胞的活性,从而发挥心肌保护作用。Objective To investigate the effect of miRNA-155 on autophagy and apoptosis of myocardial cells and Notch signaling pathway in oxygen-glucose deprivation model.Methods Establishing the model of oxygen-glucose deprivation(OGD),the cells were divided into normal control group,OGD group,OGD+miRNA-155 inhibitor negative control group and OGD+miRNA-155 inhibitor group.RT-qPCR was used to detect the expression of miRNA-155 in myocardial cells in the OGD group and the normal control group.The expression of Notch1,Hes1,Beclinl and Caspase-3 in OGD group,OGD+miRNA-155 inhibitor negative control group and OGD+miRNA-155 inhibitor group was detected by Western blots.The activity of myocardial cells in each group was detected by the CCK-8 assay.Results The result of RT-qPCR showed that the expression of miRNA-155 was significantly increased in OGD group,compared with normal control group.The results of Western blots showed that miRNA-155 inhibitor significantly increased the expression of Notch 1,HES1,Beclinl and decreased the expression of Caspase-3 in myocardial cells with oxygen-glucose deprivation.The results of CCK-8 showed that inhibition the expression of miRNA-155 could significantly increase the activity of myocardial cells with oxygen-glucose deprivation.Conclusion MiRNA-155 inhibitor exerts the myocardial protection through enhancing the expression of Notch1 and HES1,activating Notch signaling pathway,promoting autophagy,inhibitting apoptosis and increase the activity of cardiomyocytes.

关 键 词：miRNA-155 NOTCH信号通路 缺糖缺氧 自噬 凋亡 

分 类 号：R365[医药卫生—病理学]