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机构地区:[1]国家体育总局体育科学研究所,北京100061
出 处:《中国运动医学杂志》2012年第5期420-426,共7页Chinese Journal of Sports Medicine
基 金:国家体育总局体育科学研究所基本科研业务经费(09-10)
摘 要:目的:探讨大鼠力竭运动后不同时相心脏窦房结、房室结和浦肯野氏纤维代谢因子过氧化体增殖物激活型受体α(PPARα)基因和蛋白水平的表达特点,为阐明运动性心律失常发生机制提供实验依据。方法:100只健康成年雄性SD大鼠随机分为一次力竭组(4组)、2周反复力竭组(4组)及其相应的安静对照组(2组),每组10只。分别于力竭运动后即刻、4、12及24小时,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和免疫荧光方法检测PPARαmRNA和蛋白表达。结果:一次和反复力竭运动后,心脏传导系统各部位PPARαmRNA和蛋白表达均在运动后4小时下降至低谷,反复力竭后12小时,房室结PPARαmRNA和蛋白表达显著低于一次力竭后12小时(P<0.01);反复力竭后24小时浦肯野氏纤维PPARαmRNA表达显著低于一次力竭后24小时(P<0.01),其他各时相组间无明显差异(P>0.05)。结论:力竭运动后心脏传导系统各部位代谢调节因子PPARα在mRNA和蛋白水平异常低表达,且有时相性规律,易诱发传导系统能量代谢障碍,构成运动性心律失常的病理过程。Objective This paper discusses the mRNA and protein expression of PPARα on cardiac sinus node (SAN), atrioventricular (AVN) node and Purkinje's fibers at different time phrase after exhaustive exercise, and tries to provide experimental evidence for clarifying the mechanism of exercise- induced arrhythmia. Methods 100 healthy adult male SD rats were grouped into the one-time exhaustive swimming group (n = 40), the 2-week repeated exhaustive swimming group (n = 40), and the control group(n = 20). The exercise rats were sacrificed at 0,4, 12,and 24 hours after exhaustive swimming and the control rats were sacrificed at the same time as 0 hour after exhaustive swimming group. The cells of SAN,AVN and Purkinje's fiber were spotted and collected in the approach of Laser Micro dissection (LMD). The mRNA and protein expression of PPARα on the SAN, AVN and Purkinje's fiber were analyzed by real-time fluorescent quantitative PCR,immunochemistry and image analysis. Results After ex- haustive exercises,the mRNA and protein expression of PPARα on cardiac conduction system has reached the lowest level at 4 hours. Compared to one-time exercise group, the expression of mRNA and protein of PPARα on cardiac sinoatrial node and atrioventricular node increased greatly immediately af- ter repeated exhaustive exercise (P 〈 0.05, P 〈 0.01 ). The mRNA and protein expression of PPARα on cardiac atrioventricular node decreased greatly at 12 hours in repeated exhaustive exercise (P 〈 0.01 ). The mRNA and protein expression of PPARα on Purkinje's fiber decreased greatly at 24 hours in re- peated exhaustive exercise compared to one-time exercise group (P 〈 0.01 ). Conclusion The abnormal expression of PPARα mRNA and protein might cause energy metabolic obstacle after exhaustive exer- cise, and form the pathology basis of the exercise induced arrhythmia
关 键 词:力竭运动 过氧化体增殖物激活型受体Α 窦房结 房室结 浦肯野氏纤维
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