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miR-451对心肌细胞缺氧再复氧损伤的保护作用及其机制

胡笑容 谢菁 马瑞松 廖芫熙 李雪飞 江洪

山东医药2017,Vol.57Issue(17):1-3,3.
山东医药2017,Vol.57Issue(17):1-3,3.DOI:10.3969/j.issn.1002-266X.2017.17.001

miR-451对心肌细胞缺氧再复氧损伤的保护作用及其机制

Protective effect of miR-451 on anoxia/reoxygenation injury in cardiomyocytes

胡笑容 1谢菁 1马瑞松 1廖芫熙 1李雪飞 1江洪1

作者信息

  • 1. 武汉大学人民医院,武汉430060
  • 折叠

摘要

Abstract

Objective To investigate the protective effect of microRNA-451(miR-451)on anoxia/reoxygenation(A/R)injury in cardiomyotes and high mobility group box 1 protein(HMGB1)expression.Methods Neonatal rat ventricular cardiomyocytes were prepared and then subjected to A/R injury.Then they were divided into the control group(Con group),anoxia and reoxygenation group(AR group),AR+Ad-GFP group(empty virus group),AR+Ad-miR-451 group(miR-451 up-regulation group),AR+Ad-asmiR-451 group(miR-451 down-regulation group).We detected the cell viability,apoptosis rate,and the expression of Caspase-3 and HMGB1,HMGB1 mRNA.The luciferase assay was performed to further confirm MiR-451 targets for HMGB1.Results Compared with the Con group,the cell viability decreased,apoptosis index(AI)and the expression of Caspase-3,HMGB1 and HMGB1 mRNA increased in the other four groups(all P<0.05).Compared with AR group,cell viability increased,apoptosis index(AI)and the expression of Caspase-3,HMGB1 and HMGB1 mRNA decreased in the Ad-miR-451 group(all P<0.05).The luciferase assay confirmed that the 3'UTR of HMGB1 mRNA was a direct target of miR-451 in cardiomyocytes,which inhibited the expression of HMGB1.Conclusion The up-regulation of miR-451 could protect A/R injury-induced cardiomyocytes by inhibiting HMGB1 expression through miR-451.

关键词

心肌细胞/缺氧再复氧损伤/微小RNA-451/高迁移率族蛋白1

Key words

cardiomyocytes/anoxia/reoxygenation injury/microRNA-451/high mobility group box 1 protein

分类

医药卫生

引用本文复制引用

胡笑容,谢菁,马瑞松,廖芫熙,李雪飞,江洪..miR-451对心肌细胞缺氧再复氧损伤的保护作用及其机制[J].山东医药,2017,57(17):1-3,3.

基金项目

国家自然科学基金资助项目(81370308). (81370308)

山东医药

OACSTPCD

1002-266X

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