不同时相力竭运动对大鼠心肌EGR-1、CYR61及CTGF的影响
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摘要
研究目的：本研究通过力竭游泳运动模拟运动性心肌微损伤的发生,分析总结力竭后24小时内心肌不同时相心肌早期生长应答因子EGR-1(early growth response-1,EGR-1)、富半胱氨酸61(cystein rich 61,CYR61,CCN1)、结缔组织生长因子(connective tissue growth factor,CTGF,CCN2)的变化特点及规律,力图为运动性心肌微损伤的病理与发生机制的探讨提供实验依据。
研究方法：本研究以大鼠力竭游泳运动建立运动性心肌微损伤实验动物模型为基础,选用免疫荧光组织化学法和图像分析技术,研究不同力竭后心肌早期生长应答因子EGR-1、富半胱氨酸61、结缔组织生长因子的时相性变化。
研究结果：1、一次力竭运动后大鼠心肌EGR-1蛋白在运动后即刻与对照组相比显著性升高(P<0.05),运动后24小时与对照组相比呈显著性降低(P<0.05),此外,即刻组、24小时组与各时相组组间比呈显著性差异(P<0.05)。反复力竭大鼠心肌EGR-1在运动后即刻显著性高于对照组和其余各时相组(P<0.05),6至24小时各组均显著性低于对照组和一次力竭相应时相组的含量(P<0.05)。
2、一次力竭运动后大鼠心肌CYR61在运动后即刻出现峰值(P<0.05),运动后6小时出现峰谷(P<0.05),之后呈现略微上升、略微下降的变化趋势。反复力竭运动后大鼠心肌CYR61同样在即刻出现峰值(P<0.05),然后在运动后6小时出现峰谷(P<0.05),之后呈现出略微上升的变化趋势。
3、一次性和反复力竭运动后即刻,大鼠心肌CTGF含量均与相应力竭运动的对照组和6小时后各组呈显著性上升(P<0.05),之后蛋白含量均呈下降趋势,其中,一次力竭组12小时和24小时显著性降低(P<0.05)。
结论：(1)一次性和反复力竭运动后心肌EGR-1的含量有明显的时相性变化规律,呈先上升后下降的趋势,运动后即刻出现峰值,说明EGR-1作为炎症反应的起始因子,不仅介导炎症细胞的浸润引起心肌细胞损伤反应,还通过一些细胞因子促使心肌细胞凋亡,降低心肌细胞内肌浆网Ca2+转运,影响心肌收缩性,构成心肌微损伤病理与发生的机制之一。
(2)一次性和反复力竭运动后心肌CYR61含量在力竭后即刻有一个短暂上升,其反应性增高促使心肌血管生成有利于心肌供血,起到心肌细胞的保护作用；但6小时显著下降至低谷,说明CYR61对心肌细胞的保护作用非常短暂,也提示其对于心肌微损伤发生过程的影响具有双重性。
(3)一次性和反复力竭运动后心肌CTGF含量有时相性变化规律,呈先升高再降低的趋势,运动后即刻CTGF含量的增高可以促使成纤维细胞增生,构成心肌纤维化的发生因素,势必影响心肌舒张和收缩功能。力竭运动12小时后CTGF含量的降低,也说明CTGF在运动性心肌微损伤发生机制中属早期始动因子。
(4)一次性和反复力竭运动后大鼠心肌左、右心室和室间隔等部位EGR-1、Cyr61和CTGF含量无显著性差异,不同于以往研究中其他因子的变化规律。
Objective:In this study,analyzed and summarized myocardial EGR-1,CYR61 and CTGF protein in the characteristics of phase change and the rules after exhaustive through the exhaustive swimming to simulate the occurrence of exercise-induced myocardial micro-injury, in order to explore the protection mechanism and the mechanism of ventricular remodeling about exercise-induced myocardial micro-injury.
Methods:This study selected methods of immunofluorescence histochemistry and image analysis technology to study the phase changes of myocardial EGR-1,CYR61 and CTGF after exhaustive, based with exhaustive swimming exercise of rat myocardial movement to establish experimental animal models of micro-damage.
Result:(1)Myocardial EGR-1 protein content of each part of the heart were significantly increase(P<0.05) after both single bout and repeatedly exhausted exercise group,while it has significantly decrease(P<0.05) after 24hours single bout,and it has significantly lower(P<0.05) than the control group and the single bout with the same time-phasein 6,12,24hours consecutive daily exhausted exercise group.
(2) Myocardial CYR61 protein content of each part of the heart were significantly increase(P<0.05) after both single bout and repeatedly exhausted exercise group, while it has significantly decrease(P<0.05) after 6 hours single bout, and it has significantly decrease(P<0.05) in 6 hours consecutive daily exhausted exercise group.
(3) Myocardial CTGF protein content of each part of the heart were significantly increase(P<0.05) after both single bout and repeatedly exhausted exercise group, while it has significantly decrease(P<0.05) after 12,24hours in single bout. Conclusion:(1)Different exhausted exercise, various parts of myocardial EGR-1 protein content showed increase-decrease changes,EGR-1 as a key factor, can induce the cardiovascular cell apoptosis,inflammatory response,decrease the content of Ca2+,finally lead to the damage of myocardium.
(2) Different exhausted exercise, various parts of myocardial CYR61 protein content showed increase-decrease changes. CYR61 can protect from serious myocardial injury. But while CYR61 protein content decreasing, it reduce the protection to myocardium, These dual features are characterized in the damage of myocardium.
(3) Different exhausted exercise,various parts of myocardial CTGF protein content showed increase-decrease changes. CTGF play an important role in Fibrotic myocardium damage, finally lead to the damage of myocardium. And at the same time, the decreasing of the content of CTGF means that it s a immediate early factor.
(4)Different exhausted exercise, EGR-1,CYR61,CTGF protein content showed no significant differences in right ventricular, left ventricular and interventricular septum of myocardial.
研究方法：本研究以大鼠力竭游泳运动建立运动性心肌微损伤实验动物模型为基础,选用免疫荧光组织化学法和图像分析技术,研究不同力竭后心肌早期生长应答因子EGR-1、富半胱氨酸61、结缔组织生长因子的时相性变化。
研究结果：1、一次力竭运动后大鼠心肌EGR-1蛋白在运动后即刻与对照组相比显著性升高(P<0.05),运动后24小时与对照组相比呈显著性降低(P<0.05),此外,即刻组、24小时组与各时相组组间比呈显著性差异(P<0.05)。反复力竭大鼠心肌EGR-1在运动后即刻显著性高于对照组和其余各时相组(P<0.05),6至24小时各组均显著性低于对照组和一次力竭相应时相组的含量(P<0.05)。
2、一次力竭运动后大鼠心肌CYR61在运动后即刻出现峰值(P<0.05),运动后6小时出现峰谷(P<0.05),之后呈现略微上升、略微下降的变化趋势。反复力竭运动后大鼠心肌CYR61同样在即刻出现峰值(P<0.05),然后在运动后6小时出现峰谷(P<0.05),之后呈现出略微上升的变化趋势。
3、一次性和反复力竭运动后即刻,大鼠心肌CTGF含量均与相应力竭运动的对照组和6小时后各组呈显著性上升(P<0.05),之后蛋白含量均呈下降趋势,其中,一次力竭组12小时和24小时显著性降低(P<0.05)。
结论：(1)一次性和反复力竭运动后心肌EGR-1的含量有明显的时相性变化规律,呈先上升后下降的趋势,运动后即刻出现峰值,说明EGR-1作为炎症反应的起始因子,不仅介导炎症细胞的浸润引起心肌细胞损伤反应,还通过一些细胞因子促使心肌细胞凋亡,降低心肌细胞内肌浆网Ca2+转运,影响心肌收缩性,构成心肌微损伤病理与发生的机制之一。
(2)一次性和反复力竭运动后心肌CYR61含量在力竭后即刻有一个短暂上升,其反应性增高促使心肌血管生成有利于心肌供血,起到心肌细胞的保护作用；但6小时显著下降至低谷,说明CYR61对心肌细胞的保护作用非常短暂,也提示其对于心肌微损伤发生过程的影响具有双重性。
(3)一次性和反复力竭运动后心肌CTGF含量有时相性变化规律,呈先升高再降低的趋势,运动后即刻CTGF含量的增高可以促使成纤维细胞增生,构成心肌纤维化的发生因素,势必影响心肌舒张和收缩功能。力竭运动12小时后CTGF含量的降低,也说明CTGF在运动性心肌微损伤发生机制中属早期始动因子。
(4)一次性和反复力竭运动后大鼠心肌左、右心室和室间隔等部位EGR-1、Cyr61和CTGF含量无显著性差异,不同于以往研究中其他因子的变化规律。
Objective:In this study,analyzed and summarized myocardial EGR-1,CYR61 and CTGF protein in the characteristics of phase change and the rules after exhaustive through the exhaustive swimming to simulate the occurrence of exercise-induced myocardial micro-injury, in order to explore the protection mechanism and the mechanism of ventricular remodeling about exercise-induced myocardial micro-injury.
Methods:This study selected methods of immunofluorescence histochemistry and image analysis technology to study the phase changes of myocardial EGR-1,CYR61 and CTGF after exhaustive, based with exhaustive swimming exercise of rat myocardial movement to establish experimental animal models of micro-damage.
Result:(1)Myocardial EGR-1 protein content of each part of the heart were significantly increase(P<0.05) after both single bout and repeatedly exhausted exercise group,while it has significantly decrease(P<0.05) after 24hours single bout,and it has significantly lower(P<0.05) than the control group and the single bout with the same time-phasein 6,12,24hours consecutive daily exhausted exercise group.
(2) Myocardial CYR61 protein content of each part of the heart were significantly increase(P<0.05) after both single bout and repeatedly exhausted exercise group, while it has significantly decrease(P<0.05) after 6 hours single bout, and it has significantly decrease(P<0.05) in 6 hours consecutive daily exhausted exercise group.
(3) Myocardial CTGF protein content of each part of the heart were significantly increase(P<0.05) after both single bout and repeatedly exhausted exercise group, while it has significantly decrease(P<0.05) after 12,24hours in single bout. Conclusion:(1)Different exhausted exercise, various parts of myocardial EGR-1 protein content showed increase-decrease changes,EGR-1 as a key factor, can induce the cardiovascular cell apoptosis,inflammatory response,decrease the content of Ca2+,finally lead to the damage of myocardium.
(2) Different exhausted exercise, various parts of myocardial CYR61 protein content showed increase-decrease changes. CYR61 can protect from serious myocardial injury. But while CYR61 protein content decreasing, it reduce the protection to myocardium, These dual features are characterized in the damage of myocardium.
(3) Different exhausted exercise,various parts of myocardial CTGF protein content showed increase-decrease changes. CTGF play an important role in Fibrotic myocardium damage, finally lead to the damage of myocardium. And at the same time, the decreasing of the content of CTGF means that it s a immediate early factor.
(4)Different exhausted exercise, EGR-1,CYR61,CTGF protein content showed no significant differences in right ventricular, left ventricular and interventricular septum of myocardial.
引文
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