刘向辉,郝选明.间歇运动对自发性高血压大鼠心血管内皮细胞的保护作用[J].北京体育大学学报,2012,35(8):71-.
间歇运动对自发性高血压大鼠心血管内皮细胞的保护作用
Protective Effects of Interval Exercise Training on Vascular Endothelial Cells in Spontaneous Hypertensive Rat
投稿时间:2011-04-01  
DOI:
中文关键词:  关键词:高血压  间歇运动  血管内皮细胞  循环内皮祖细胞
英文关键词:Key words: hypertension  interval training  vascular endothelial cells  circulating endothelial progenitor cells
基金项目:基金项目:湖南省全民健身服务体系建设研究基地资助项目(湘哲社领[2010]14号);广东省普通高校人文社会科学研究基地重大项目(07JDXM89002)。
作者单位
刘向辉 邵阳学院体育系湖南 邵阳 422000 
郝选明 华南师范大学体育科学学院广东 广州 510006 
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中文摘要:
      摘 要:目的:探讨间歇运动对自发性高血压大鼠(SHR)胸主动脉的心血管内皮细胞的保护作用。方法:20只11周龄的自发性高血压大鼠随机分为运动组和对照组,运动组进行连续10周的间歇运动。分别于训练前后测试血压、血脂,运动10周后通过扫描电镜观察胸主动脉的内皮细胞层,测量血液中内皮细胞的数量,同时测定循环内皮祖细胞(CEPCs)的数量及增殖能力、黏附能力及凋亡情况。结果:运动组SHR胸主动脉内皮细胞层受损程度轻于对照组;运动组循环内皮细胞数量与CEPCs凋亡率低于对照组(P<0.05),而CEPCs数量、CEPCs增殖能力、CEPCs黏附能力均高于对照组(P<0.05)。结论:长期的间歇运动能增加SHR的CEPCs数量、提高CEPCs功能、降低CEPCs的凋亡、增强CEPCs对血管内皮细胞的修复能力,对高血压大鼠的血管内皮细胞具有保护作用。
英文摘要:
      Abstract:Objective: To investigate the effect of interval exercise training on vascular endothelial cells in spontaneous hypertensive rat (SHR). Methods: Twenty male,11-week-old SHR were randomly assigned to either an interval training group (IE) or a sedentary control group(CR). Blood pressure and blood lipid were measured before and after training. On the 10th week, scanning electron microscopy was used to observe the damage of aortic endothelial cells. The circulatory endothelial cell count, CEPCs count, CEPCs proliferation ability, CEPCs adhesion ability and CEPCs apoptosis were also measured respectively. Results: The injury degree of endothelial cells in IE group was decreased compared with that CR group. The numbers of circulatory endothelial cells and the CEPCs apoptosis rate in IE group were lower than that of CR group(P<0.05). While the numbers of CEPCs , the proliferative abilities of CEPCs and the adhesion of CEPCs were higher than that of CR group(P<0.05). Conclusion: Interval exercise training has direct protective effects on endothelial cells, by increasing CEPCs count, improving the function of CEPCs, reducing CEPCs’ apoptosis and markedly enhancing the reparation ability of CEPCs to endothelial cells.
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