| 注册
首页|期刊导航|山东医药|Nogo-A蛋白在大鼠心肌细胞中的表达变化及其在细胞缺氧性凋亡中的作用

Nogo-A蛋白在大鼠心肌细胞中的表达变化及其在细胞缺氧性凋亡中的作用

程亮 易蔚 任凯 裴建明

山东医药2013,Vol.53Issue(22):13-15,21,4.
山东医药2013,Vol.53Issue(22):13-15,21,4.DOI:10.3969/j.issn.1002-266X.2013.22.005

Nogo-A蛋白在大鼠心肌细胞中的表达变化及其在细胞缺氧性凋亡中的作用

Expression of Nogo-A protein in rat cardiomyocytes and its effect on hypoxia-induced apoptosis

程亮 1易蔚 1任凯 1裴建明2

作者信息

  • 1. 第四军医大学西京医院,西安710032
  • 2. 第四军医大学生理学教研室
  • 折叠

摘要

Abstract

Objective To investigate the expression of Nogo-A protein in rat cardiomyocytes and its effect on hypoxiainduced apoptosis.Methods ① Nogo-A protein expression was determined in adult rat cardiomyocytes by using immunohistochemistry and Western blot.② The acutely isolated myocardial cells were divided into three groups:the control group,model group and intervention group.To establish the hypoxia-induced myocardial cell apoptosis models in the model group and intervention group,the intervention group was treated with the anti-Nogo-A antibodies before the modeling.The apoptosis,the expre.ssion of Nogo-A protein,Caspase-3 and Caspase-12 in three groups were observed.Resets ① Adult cardiomyocytes:the expression of Nogo-A protein was positive.② Cardiomyocytes under hypoxia:the expression of NogoA protein was positive; the intervention group and the model group appeared apoptotic cells,but the intervention group was significantly less than the model group; the positive rates of Caspase-3 and Caspase-12 expression were significantly higher in the intervention group and model group than those in the control group,but the intervention group was significantly lower than the model group,P < 0.05.Conclusions There was a large amount of expressed Nogo-A protein in myocardial cells.Nogo-A protein may be involved in the hypoxia-induced apoptosis of myocardial cells.

关键词

Nogo-A蛋白/心肌细胞/缺氧性凋亡

Key words

Nogo-A protein/ cardiomyocytes/ hypoxic apoptosis

分类

医药卫生

引用本文复制引用

程亮,易蔚,任凯,裴建明..Nogo-A蛋白在大鼠心肌细胞中的表达变化及其在细胞缺氧性凋亡中的作用[J].山东医药,2013,53(22):13-15,21,4.

基金项目

陕西省社发公关资助项目(2012K15-01-05). (2012K15-01-05)

山东医药

OACSTPCD

1002-266X

访问量0
|
下载量0
段落导航相关论文