The Journal of Practical Medicine ›› 2021, Vol. 37 ›› Issue (3): 304-307.doi: 10.3969/j.issn.1006⁃5725.2021.01.006

• Basic Research • Previous Articles     Next Articles

Effects of miRNA⁃155 on Notch signaling pathway and autophagy and apoptosis of myocardial cells in oxy⁃ gen⁃glucose deprivation model

CHEN Xiyan,MA Yanjuan,NIU Lidan,YANG Yaqin,YANG Feiyun,SHI Jin⁃he.
  

  1. Department of Emergency,the First Affiliated Hospital of Xinxiang Medical University,Weihui 453100,China
  • Online:2021-02-10 Published:2021-02-10
  • Contact: SHI Jinhe E⁃mail:sjh4402901@163.com

Abstract:

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,Beclin1 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 Notch1,HES1,Beclin1 and decreased the expression of Caspase⁃3 in myocardial cells with oxygen⁃glucose deprivation. The results of CCK⁃8 showed that inhi⁃ bition 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 

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