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.
作者
陈希妍
马彦娟
牛丽丹
杨亚琴
杨飞云
石金河
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)
出处
《实用医学杂志》
CAS
北大核心
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)。
