摘要
目的:探讨力竭运动后不同时相心脏窦房结、房室结和浦肯野氏纤维细胞炎性因子TNF-α基因和蛋白水平的表达特点,为运动性心律失常发生机制的阐明提供实验依据。方法:100只健康成年雄性SD大鼠随机分为一次和反复力竭组及相应的对照组,每组10只。分别于力竭运动后0、4、12及24h应用激光显微切割技术定位并收集窦房结、房室结和浦肯野氏纤维细胞,采用实时荧光定量PCR和免疫荧光方法研究细胞炎性因子TNF-α的mR-NA和蛋白表达的变化。结果:一次力竭运动后窦房结和房室结的TNF-αmRNA和蛋白表达规律基本一致,呈先升高后下降的趋势,在运动后即刻明显高于对照组(P<0.01)。浦肯野纤维TNF-αmRNA和蛋白表达呈先下降后上升趋势,在运动后4h明显低于对照组(P<0.01)。反复力竭运动后窦房结、房室结和浦肯野纤维的TNF-αmRNA和蛋白表达呈下降趋势,与对照组相比,窦房结和浦肯野纤维在运动后12h最明显,房室结在运动后24h最明显(P<0.01)。结论:一次力竭运动后即刻窦房结和房室结炎性因子TNF-α在mRNA和蛋白水平均大量表达,易引起心脏传导系统炎性细胞浸润,细胞间质增殖乃至纤维化和损伤,势必影响正常心脏的起搏和传导,构成运动性心律失常的病理基础。而反复力竭运动致心脏传导系统各部位细胞累积损伤,作为细胞炎性因子TNF-α在mRNA和蛋白水平未表现出明显的应激性反应,呈现出低表达趋势。
Objective：To discuss the gene and protein expression characters of TNF-α of cardiac sinus node, atrioventricular node and Purkinje fibers at different time-phrase after exhaustive exercise, providing experimental evidence for clarifying the mechanism of exercise-induced ar rhythmia. Method： 100 healthy adult male SD rats were grouped into 10 groups （10 rats for each group） as 4 groups of one-time exhaustive swimming group （n = 40）, 4 groups of 2-week repeated exhaustive swimming group （n= 40） and 2 control groups （n= 20）. Rats were sacrificed at 0,4,12, and 24 hours after exhaustive swimming, then Laser microdissection （LMD） and immune fluorescent histochemical were underwent according to time-phrase. The SAN, AVN and Purkinje＇s fiber cells were spotted and collected in the approach of Laser Microdissection （LMD）. The mRNA and protein expression of TNF-α on the SAN, AVN and Purkinje ＇s fiber cells were analyzed by real-time fluorescent quantitative PCR, immunochemistry and image analysis. Results：Compared to control group, the expression of mRNA and protein of TNF-α on cardiac sinoatrial node and atrioventricular node increased greatly immediately after two exhaustive exercise（P〈0.01 ）. The expression of mRNA and protein of TNF-α on cardiac Purkinje fiber dropped markedly 4 hours after one-time exhaustive exercise（P〈0.01 ）. The expression of mRNA and protein of TNF-α on heart conduction system declined significantly after repeated exhaustive exercise, especially at 12 hours after exercise on sinoatrial node and atrioventricular node and 24 hours on Purkinjes fiber cells（P〈0.01）. Conclusion：After onetime exhaustive exercise, the mRNA and protein of TNF-α greatly expressed on sinoatrial node and atrioventricular node, causes inflammation and proliferation on fiber cells, leading to the cardiac sinus pacing and sinus electrical conduction abnormalities, which is one of the factors of arrhythmia. Repeated exhaustive exercise causes irreversible damage on car
出处
《体育科学》
CSSCI
北大核心
2012年第7期32-38,共7页
China Sport Science
基金
国家体育总局体育科学研究所基本科研业务费资助项目(基本10-01)
关键词
力竭运动
肿瘤坏死因子α
窦房结
房室结
浦肯野氏纤维
鼠
动物实验
exhaustive swimming
TNF-α
cardiac sinoatrial node
atrioventricular node Purkinje＇s fiber rat animal experiment
