Up-regulation of Thioredoxin 1 by aerobic exercise training attenuates endoplasmic reticulum stress and cardiomyocyte apoptosis following myocardial infarction  

作　　者：Mengxin Cai Zujie Xu Wenyan Bo Fangnan Wu Wenpu Qi Zhenjun Tian 

机构地区：[1]Institute of Sports Biology,School of Physical Education,Shaanxi Normal University,Xi’an,Shaanxi,China

出　　处：《Sports Medicine and Health Science》2020年第3期132-140,共9页运动医学与健康科学（英文）

基　　金：supported by National Natural Science Foundation of China(Grant No.31701039,31671240);the Fundamental Research Funds for the Central Universities,Shaanxi Normal University(Grant Number GK201803096).

摘　　要：Exercise training(ET)has been reported to reduce oxidative stress and endoplasmic reticulum(ER)stress in the heart following myocardial infarction(MI).Thioredoxin 1(Trx1)plays a protective role in the infarcted heart.However,whether Trx1 regulates ER stress of the infarcted heart and participates in ET-induced cardiac protective effects are still not well known.In this work,H9c2 cells were treated with hydrogen peroxide(H_(2)O_(2))and recombinant human Trx1 protein(TXN),meanwhile,adult male C57B6L mice were used to establish the MI model,and subjected to a six-week aerobic exercise training(AET)with or without the injection of Trx1 inhibitor,PX-12.Results showed that H_(2)O_(2)significantly increased reactive oxygen species(ROS)level and the expression of TXNIP,CHOP and cleaved caspase12,induced cell apoptosis;TXN intervention reduced ROS level and the expression of CHOP and cleaved caspase12,and inhibited cell apoptosis in H_(2)O_(2)-treated H9c2 cells.Furthermore,AET up-regulated endogenous Trx1 protein expression and down-regulated TXNIP expression,restored ROS level and the expression of ER stress-related proteins,inhibited cell apoptosis as well as improved cardiac fibrosis and heart function in mice after MI.PX-12 partly inhibited the AET-induced beneficial effects in the infarcted heart.This study demonstrates that Trx1 attenuates ER stress-induced cell apoptosis,and AET reduces MI-induced ROS overproduction,ER stress and cell apoptosis partly through up-regulating of Trx1 expression in mice with MI.

关 键 词：Endoplasmic reticulum stress Myocardial infarction Exercise training Thioredoxin 1 Oxidative stress 

分 类 号：R73[医药卫生—肿瘤]