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比索洛尔预处理对缺氧/复氧诱导的H9c2细胞损伤的影响

习明明 刘晶 谢亮 宫剑滨

南方医科大学学报2016,Vol.36Issue(9):1198-1203,6.
南方医科大学学报2016,Vol.36Issue(9):1198-1203,6.DOI:10.3969/j.issn.1673-4254.2016.09.06

比索洛尔预处理对缺氧/复氧诱导的H9c2细胞损伤的影响

Effects of bisoprolol pretreatment on hypoxia/reoxygenation-induced injury in H9c2 cardiomyocytes

习明明 1刘晶 2谢亮 2宫剑滨2

作者信息

  • 1. 泰州市人民医院内科,江苏 泰州 225300
  • 2. 南京大学医学院附属金陵医院 南京军区南京总医院 心脏内科,江苏 南京 210002
  • 折叠

摘要

Abstract

Objective To investigated the effects of bisoprolol pretreatment on hypoxia/reoxygenation (H/R)-induced injury in H9c2 cardiomyocytes. Methods Cultured H9c2 cells were exposed to hypoxia for 6 h followed by reoxygenation for 2 h with or without pretreatments with bisoprolol or bisoprolol+LY294002. The cell survival was measured by MTT assay, and the cell apoptosis and levels of radical oxygen species (ROS) were evaluated with flow cytometry. The protein levels of phosphyorylated AKT and phosphorylated GSK3βin the cells were determined by Western blotting. Results Compared with the normal control cells, the cells exposed to H/R injury showed significantly decreased cell survival and increased cell apoptosis and ROS production; pretreatment of the cells with bisoprolol significantly decreased the cell apoptotic rates and ROS production and obviously enhanced the cell survival and protein levels of p-AKT and p-GSK3βin the exposed cells. The protective effect of bsioprolol against H/R-induced cell injury was significantly attenuated by LY294002. Conclusion Bisoprolol can protect H9c2 cells against H/R-induced injury and oxidative stress by activating PI3K/AKT/Gsk-3βpathway to increase the phosphorylation of AKT and GSK3βand reduce ROS production.

关键词

比索洛尔/缺氧/复氧损伤/H9c2/心肌保护/PI3K/AKT/GSK3β

Key words

bisoprolol/hypoxia/reoxygenation injury/H9c2/myocardial protection/PI3K/AKT/GSK3β

引用本文复制引用

习明明,刘晶,谢亮,宫剑滨..比索洛尔预处理对缺氧/复氧诱导的H9c2细胞损伤的影响[J].南方医科大学学报,2016,36(9):1198-1203,6.

基金项目

国家自然科学基金(81400238) Supported by National Natural Science Foundation of China (81400238) (81400238)

南方医科大学学报

OA北大核心CSCDCSTPCDMEDLINE

1673-4254

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