【摘要】 目的:探讨运动性心肌损伤中大鼠缝隙连接蛋白43(Cx43)基因和蛋白表达的变化。方法:SD大鼠50只随机分为对照组(C组)和力竭运动组(EE组),大强度力竭跑台运动建立运动性心肌损伤模型。用苏木素-碱性品红-苦味酸(HBFP)染色方法观察大鼠心肌缺血缺氧改变,心肌肌钙蛋白I(cTnI)含量用免疫化学发光法进行检测,心肌Cx43 mRNA的表达分布采用原位杂交方法,用实时荧光定量PCR法检测心肌Cx43 mRNA表达,用免疫组织化学方法观察心肌Cx43表达分布,用Western免疫印迹法检测Cx43蛋白表达。结果:与C组相比,EE组心肌缺血缺氧面积明显增加,血清cTnI含量明显升高,Cx43原位杂交信号有减弱趋势,免疫阳性反应明显减弱,可见少量Cx43免疫阳性分布于心肌细胞闰盘和侧对侧连接处,Cx43蛋白表达水平明显降低。结论:1)大强度力竭运动导致大鼠运动性心肌损伤,该损伤能引起心肌Cx43分布模式的改变,提示心肌Cx43是导致心功能异常并引发运动性心肌损伤的结构基础。2)心肌Cx43蛋白表达在运动性心肌损伤中降低,提示力竭运动可能通过引起Cx43去磷酸化而引起Cx43表达降低,从而导致运动性心肌损伤的发生。更多还原

【Abstract】 Objective:To probe into connexin 43( Cx43) gene and protein expression during exercise-induced myocardial injury.Methods:50 SD rats were divided into control group( group C) and exhaustive exercise group( group EE) randomly.High intensity exhaustive exercise on treadmill to establish exercise-induced myocardial injury model.Using hematoxylin basic fuchsin picric acid( HBFP) staining method to observe the change of myocardial ischemia and hypoxia.Immune chemiluminescence were used to detect cardiac troponin I( cTnI) content.Distribution of myocardial Cx43 mRNA were observed by in situ hybridization method,and the expression of myocardial Cx43mRNA were detected by real-time fluorescent quantitative PCR method.Distribution of myocardial Cx43 were observed by immunohistochemical method.And the expression Cx43 protein were detected by Western blotting.Results:Compared with C group,EE group myocardial ischemia and hypoxia area increased.The content of cTnI in serum increased significantly.Cx43 in situ hybridization signals have weakening trend,and Cx43 immunoreactivity significantly decreased.A small amount of Cx43 immunoreactive distribution in intercalated disk and lateral connections on the side.The expression of Cx43 protein levels decreased significantly.Conclusion:1) High intensity exhaustive exercise caused exercise-induced myocardial injury.The injury can cause myocardial Cx43 distribution patterns change,pointed out that myocardial Cx43 is the structural basis of abnormal heart function and cause exercise-induced myocardial injury.2) Myocardial Cx43 protein expression reduced in exercise-induced myocardial injury,indicated that the exhaustive exercise may decreased the gap junctional expression of Cx43 through myocardial Cx43dephosphorylation and then exercise-induced myocardial injury happened.更多还原