低硒大鼠心肌线粒体STAT3的活性变化及其与心肌损伤的关系  

Change of cardiac mitochondrial STAT3 activity in rats with selenium deficiency and its relation with myocardial injury

作　　者：张明[1] 魏瑾[1] 潘晓青[1] 单虎[1] 闫蕊[1] 薛嘉虹[1] 朱延河[1] 林琳[1] 

机构地区：[1]西安交通大学医学院第二附属医院心内科,陕西西安710004

出　　处：《南方医科大学学报》2013年第7期967-971,共5页Journal of Southern Medical University

基　　金：国家自然科学基金(30771862;81170209;81100210);陕西省科技攻关项目(2007K13-03)~~

摘　　要：目的研究低硒大鼠心肌线粒体中信号转导和转录激活子3(STAT3)的磷酸化活性及其在心肌损伤中的作用。方法 36只大鼠随机分为正常对照组(n=18)和低硒模型组(n=18)。分别于喂养第20、30、40周时颈动脉插管测其心功能;电镜观察心肌线粒体结构的损伤;提取心肌线粒体,以比色法测定琥珀酸脱氢酶和细胞色素C氧化酶的活性,Western blotting检测线粒体中STAT3和p-STAT3的表达。结果(1)与对照组相比,低硒组大鼠心脏收缩及舒张功能均降低、心肌线粒体结构与功能受损,且随着低硒喂养时间的延长而损伤加重(P<0.05);(2)与对照组相比,低硒组大鼠心肌线粒体中STAT3的活性(p-STAT3/STAT3)显著降低,且随着低硒喂养时间的延长而呈下降趋势(P<0.05);(3)Pearson直线相关性分析显示,心肌线粒体STAT3的活性与左心室峰值收缩压、左心室内压最大上升速率、琥珀酸脱氢酶、细胞色素C氧化酶呈正相关(P<0.01)。结论低硒可下调大鼠心肌线粒体STAT3的活性,参与心肌线粒体损伤和心功能的衰竭。Objective To study the phosphorylation activity of mitochondrial signal transducer and activator of transcription 3 （STAT3） in the myocardium of rats with selenium deficiency and its association with myocardial injury. Methods Thirty- six rats were randomized into normal control group （n=18） and selenium deficiency model group （n=18） for feeding with normal and low-selenium chow, respectively, for 20, 30 and 40 weeks. The cardiac function of the rats was evaluated by carotid artery intubation, and the damage of cardiac mitochondria was observed under electron microscopy. The cardiac mitochondria were extracted for assessing succinate dehydrogenase and cytochrome C oxidase activities, and the protein expressions of phosphorylated and total STAT3 were detected. Results Compared with the corresponding control groups, the rats in the model group showed significantly decreased cardiac function with obvious structural and functional damage of the cardiac mitochondria （P0.05）, which aggravated as the low-selenium feeding time extended （P0.05）. The rats in the model group also showed significantly decreased mitochondrial STAT3 activity （p- STAT3/STAT3） in the myocardium as the low- selenium feeding time prolonged （P0.05）. Pearson linear correlation analysis showed that the activity of cardiac mitochondrial STAT3 had positive correlations with the left ventricular systolic pressure, maximal increased rate of the left ventricular pressure, and the activities of succinate dehydrogenase and cytochrome C oxidase （P0.01）. Conclusion Selenium deficiency down-regulates the activity of mitochondrial STAT3 in rat heart to contribute to cardiac mitochondrial injury and the progression of heart failure.

关 键 词：低硒 心肌线粒体 信号转导和转录激活子3 心功能 

分 类 号：R363[医药卫生—病理学]