| 摘要: |
| 【目的】研究运动对大鼠心肌细胞及一氧化氮合酶的影响，探讨运动引起心肌细胞凋亡的可能机制。【方法】通过游泳训练建立大鼠有氧训练组和力竭过度训练组模型，以常规饲养大鼠为对照，检测各组大鼠心脏质量与心系数（心脏质量/体质量）的变化，采用Western blot检测心肌细胞中p53蛋白的表达，DNA ladder法检测心肌组织细胞的凋亡，并测定各组大鼠心肌与血清中的NO含量及结构型NOS（cNOS）、诱导型NOS（iNOS）活性。【结果】力竭过度训练组大鼠心脏质量和心系数增加，心肌细胞中p53蛋白的表达显著增加，与过度训练时大鼠心肌细胞凋亡基因的调控有关。DNA ladder检测结果显示，有氧训练组大鼠心肌与血清中的cNOS活性升高，有少量的NO生成，对大鼠心血管系统产生了良性影响，使大鼠心血管系统功能增强；而力竭过度训练组出现了明显的凋亡条带，长期的过度负荷使大鼠心肌与血清中的iNOS活性升高，产生的较多NO对细胞具有毒性作用。【结论】不适宜的运动负荷会促使大鼠心肌细胞凋亡，NO可能参与了心肌的损害过程。 |
| 关键词: 心肌细胞 细胞凋亡 p53蛋白 一氧化氮合酶 大鼠 |
| DOI： |
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| 基金项目:安徽高校省级自然科学研究项目（KJ2012Z170) |
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| Effect of exercise on myocardial cell and nitric oxide synthase in rats |
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JIANG Lei, ZHOU Zhenmaol, XIA Meiyan,et al
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Anhui Medical University
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| Abstract: |
| 【Objective】This study investigated the mechanism of myocardial apoptosis and researched the effects of exercise on apoptosis of myocardial cell and nitric oxide synthase in rats.【Method】Aerobic exercise group and overtraining group models were established based on swimming training.The rats in regular feeding group were set as control to detect changes of heart weight and heart coefficient in other groups.The expressions of p53 protein were detected by Western blot.The apoptosis of myocardial cell were detected by DNA ladder in tissue sections.Determination of NO content,cNOS and iNOS activity in rats myocardial and serum were measured by kit.【Result】The heart weight and heart coefficient of rats in overload training group increased.The expression of p53 protein increased significantly in cardiac muscle cell after overtraining,which might have relation to genetic controls on apoptosis in myocardial cell.DNA ladder results showed that it had noticeably apoptosis strips after overload training.cNOS activity in myocardial and serum of rats in the aerobic exercise group increased,and generate a small amount of NO was generated,positively affecting cardiovascular system,but long term overload training could lead to too much NO,which had toxic effect on cell.【Conclusion】Inappropriate exercises load will result in the increase of myocardial apoptosis,and NO may be involved in the process of myocardial damage. |
| Key words: myocardial cell cell apoptosis p53 protein nitric oxide synthase rat |
