钙网蛋白介导线粒体损伤在高糖诱导心肌细胞凋亡中的作用  被引量:7

Role of calreticulin-induced mitochondrial damage in high glucose-induced apoptosis of myocardial cells

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作  者:闫蕊[1,2] 单虎[1,2] 林琳[1,2] 刁佳宇[1,2] 张明[3] 朱延河[4] 谭武红[4] 魏瑾[1,2] 

机构地区:[1]西安交通大学第二附属医院心血管内科,陕西西安710004 [2]西安交通大学第二附属医院地方病科,陕西西安710004 [3]西安交通大学第二附属医院呼吸内科,陕西西安710004 [4]西安交通大学环境与疾病相关基因教育部重点实验室,微量元素与地方病卫生部重点实验室,陕西西安710061

出  处:《中国病理生理杂志》2015年第6期967-972,共6页Chinese Journal of Pathophysiology

基  金:国家自然科学基金资助项目(No.81170209;No.30771862)

摘  要:目的:观察高糖培养对心肌细胞钙网蛋白(calreticulin,CRT)表达的变化、线粒体功能和细胞凋亡的影响。方法:将培养的AC-16人心肌细胞随机分为正常糖浓度组、高糖组、高糖+CRT siRNA(small interfering RNA)组及等渗组,分别测定各组心肌细胞凋亡率、细胞内活性氧水平、线粒体功能和CRT表达水平的变化。结果:与正常糖浓度培养的心肌细胞相比,高糖组心肌细胞凋亡率增加,活性氧生成增多,线粒体膜电位及呼吸链酶活性降低,同时CRT表达升高;CRT siRNA可以减轻高糖组心肌细胞线粒体损伤,但细胞内活性氧的生成与高糖组相比未见显著差异。结论:CRT介导的线粒体损伤可能参与高糖时心肌细胞凋亡的增加。AIM:To observe the effect of high glucose on the protein expression of calreticulin ( CRT) and its association with cell apoptosis and mitochondrial dysfunction in the cardiomyocytes.METHODS: AC-16 cardiomyocytes were randomly divided into normal glucose group, high glucose group, high glucose+CRT siRNA group and isotonic con-trol group.The cell apoptotic rate, reactive oxygen species (ROS), mitochondrial membrane potential level, respiratory enzyme activity, and protein expression of CRT were observed.RESULTS: Compared with the cardiomyocytes in normal glucose group, the apoptotic rate and ROS production of cardiomyocytes increased in high glucose group, accompanying with the decreases in the mitochondrial membrane potential level and enzyme activitiy of the respiratory chain.The protein expression of CRT was significantly increased in high glucose group.However, compared with high glucose group, high glucose+CRT siRNA decreased the expression of CRT and attenuated the damage of mitochondria, but CRT siRNA did not reduce the ROS level in cardiomyocytes.CONCLUSION:High glucose brings about CRT over-expression to induce mito-chondrial injury, thus increasing myocardial apoptosis.

关 键 词:高糖 钙网蛋白 线粒体损伤 细胞凋亡 

分 类 号:R541.8[医药卫生—心血管疾病] R363[医药卫生—内科学]

 

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