内质网应激在晚期糖基化终产物诱导心肌细胞损伤中的作用

摘要

目的:研究晚期糖基化终产物(AGEs)对原代培养SD乳鼠心肌细胞的损伤,探讨内质网应激在AGEs诱导心肌细胞损伤中的作用.方法:原代培养SD大鼠乳鼠心肌细胞,随机分为对照组、AGEs组.MTT法检测心肌细胞存活率,Western blot法检测内质网应激蛋白GRP 78和CHOP蛋白表达水平.结果:与对照组相比,AGEs具有损伤心肌细胞的作用,并呈现剂量和时间依赖性；AGEs可以诱导内质网应激相关蛋白GRP 78和CHOP的高表达,并呈现剂量依赖性增加.结论:AGEs可以导致心肌细胞损伤,GRP 78和CHOP蛋白表达水平升高,提示内质网应激通路可能参与了AGEs诱导的心肌细胞损伤.%Objective:To investigate the effect ofendoplasmic reticulum (ER) stress on the process of advanced glycosylation end products (AGEs)-induced neonatal rat cardiomyocyte injury.Methods:Cultured neonatal rat cardiomyocytes were randomly divided into control group and AGEs group.MTT assay was used to detect cell viability.Protein expressions of GRP 78 and CHOP were determined by western blot.Results:Compared with control group,AGEs resulted in eardiomyocyte injury,which was in a time-and concentration-dependent manner.AGEs activated GRP 78 and CHOP,which was in a concentration dependent manner.Conclusions:AGEs induces cardiomyocyte injury,and upregulates protein expressions of GRP 78 and CHOP.It demonstrates that endoplasmic reticulum stress might play an important role in the process of AGEs-induced cardiomyocyte injury.