低硒大鼠心肌线粒体硫氧还蛋白2的动态表达和心肌的损伤情况

 目的：检测低硒大鼠心肌线粒体中硫氧还蛋白2（thioredoxin 2,Trx2）的蛋白表达水平，观察在体心功能及心肌细胞凋亡情况，分析Trx2与心功能及心肌细胞凋亡指数之间的相关性，探讨Trx2在心肌损伤中的作用。方法：构建低硒大鼠模型，以常硒组为对照，分别于喂养20周、30周和40周时颈动脉插管测其心功能；提取心肌线粒体，Western blotting法检测线粒体中Trx2的表达水平；免疫组织化学技术（SP法）对Fas相关死亡结构域蛋白（FADD）进行原位染色，衡量心肌细胞凋亡情况。结果：（1）各时点对照组大鼠心肌线粒体Trx2的表达无明显差异，低硒组与相应时点的对照组相比Trx2表达均降低，且随低硒喂养时间延长降低更为明显，差异显著（P<0.05）；（2）与对照组相比，低硒组大鼠心脏收缩及舒张功能均降低，以收缩功能指标--左室收缩压（left ventricular systolic pressure，LVSP）和左心室内压最大上升速率（maximum rate of left ventricular pressure rise，+dp/dt_max）降低更为明显（P<0.05）；免疫组化染色显示，随着喂养时间的延长，低硒组大鼠心肌细胞凋亡加重；（3）相关性分析显示，Trx2与LVSP和+dp/dt_max呈正相关，与心肌细胞凋亡指数呈负相关（P<0.01）。结论：低硒可通过影响大鼠心肌线粒体中Trx2蛋白的表达，参与心脏功能减退和心肌细胞凋亡；线粒体Trx2对心肌细胞具有保护作用。

Dynamic expression of thioredoxin 2 in myocardial mitochondria in selenium-deficiency rats during myocardial injury

AIM: To investigate the dynamic expression of thioredoxin 2 (Trx2) protein in the myocardial mitochondria under the condition of selenium deficiency. METHODS: A model of selenium deficiency was made using two-week-old SD rats. When the rats were fed for 20 weeks, 30 weeks and 40 weeks, the cardiac functions were detected by carotid artery intubation. The myocardial mitochondria were also extracted, and the protein expression of mitochondrial Trx2 was measured by Western blotting. The method of immunohistochemistry was used to detect Fas-associated death domain protein (FADD,a death marker protein) for determining the apoptosis of myocardial cells. The correlation between Trx2 and left ventricular systolic pressure (LVSP), maximum rate of left ventricular pressure rise(+dp/dtmax) and apoptotic index of the myocardial cells was analyzed. RESULTS: Compared with the corresponding period of normal control group, the expression of Trx2 protein in the selenium-deficiency rats was reduced. The expression of Trx2 protein was continuously reduced as the time of selenium deficiency prolonged. As the time of low-selenium feeding was going on, the systolic and diastolic functions of the heart were impaired, and the number of apoptotic myocardial cells was increased. The correlation analysis indicated that Trx2 had positive correlations with LVSP and +dp/dtmax, and had a negative correlation with the apoptotic index of myocardial cells. CONCLUSION: Selenium deficiency affects the expression of Trx2 protein,and causes impaired cardiac functions and the apoptosis of myocardial cells. Trx2 has a protective effect on myocardial cells.