运动训练对心肌线粒体途径miR-30-p53-Drp-1凋亡通路的影响

发布时间：2018-01-20 11:18

本文关键词： 游泳运动心肌线粒体微小RNA 凋亡　出处：《中国运动医学杂志》2015年02期 　论文类型：期刊论文

【摘要】：目的:心肌线粒体凋亡途径存在mi R-30-p53-Drp-1调节通路。本研究观察游泳运动训练对小鼠心肌mi R-30和下游靶蛋白的影响,探讨运动干预心肌凋亡的分子机制。方法:雄性C57BL/6小鼠随机分为安静组(SE组)、训练组1(ET1组)、训练组2(ET2),7只/组。SE组不运动,ET1组进行8周递增负荷游泳训练,5天/周,1次/天,第1周30 min/次,每周增加10 min,第7、8周时间维持在90 min;ET2组前5周和ET1组相同,后3周每次时间和ET1组相同,但2次/天。提取心肌,TUNEL检测评价心肌凋亡指数,应用RT-PCR和Western blotting技术测定mi R-30b和蛋白表达。结果:相比SE组,ET1组心肌凋亡指数无显著性变化(P0.05),mi R-30b表达显著性升高(P0.05),p53蛋白表达显著性下降(P0.01),Drp-1蛋白表达下降,但无统计学意义(P0.05);相比SE组,ET2心肌凋亡指数显著下降(P0.01),mi R-30b表达显著升高(P0.01),p53和Drp-1蛋白表达也显著下降(P0.01)。结论:ET2组中等强度游泳负荷能够更明显抑制心肌凋亡水平,整体上降低mi R-30b-p53-Drp-1通路促凋亡信号强度;而ET1组小强度游泳负荷尽管显著改变mi R-30b、p53表达,但不能对心肌凋亡水平产生明显影响。
[Abstract]:Objective: to investigate the effects of swimming exercise training on myocardial mi R-30 and downstream target proteins in mice. Methods: male C57BL / 6 mice were randomly divided into quiet group (SE group), training group (1) and training group (2). 7 rats / group. Group SE: exercise without exercise and ET1 group were treated with 8 weeks incremental load swimming training for 5 days per week, 30 minutes per week for the first week, 10 minutes per week, and 7 hours per week. The time of 8 weeks was maintained at 90 mins. The first 5 weeks of ET2 group was the same as that of ET1 group, and the time of the third week was the same as that of ET1 group, but twice a day. The myocardial apoptosis index was evaluated by Tunel. The expression of miR-30b and protein was measured by RT-PCR and Western blotting. Results: compared with SE group. There was no significant change in myocardial apoptosis index in ET1 group. The expression of Drp-1 protein decreased, but there was no significant difference between the two groups. Compared with SE group, myocardial apoptosis index of ET2 decreased significantly (P 0.01) and the expression of R-30b increased significantly (P 0.01). The expression of p53 and Drp-1 protein also decreased significantly (P 0.01). Conclusion moderate intensity swimming load can significantly inhibit myocardial apoptosis in the group of 2: ET2. The apoptotic signal intensity of MI R-30b-p53-Drp-1 pathway was decreased. However, the low intensity swimming load in ET1 group did not significantly affect the myocardial apoptosis level, although it significantly changed the expression of mi R-30b p53.
【作者单位】：唐山师范学院体育系;
【基金】：河北省高等学校科学技术研究项目(Z2014121) 唐山师范学院科学研究基金项目(2013D03)
【分类号】：R87
【正文快照】： 凋亡即细胞程序性死亡,是由基因控制的细胞主动性死亡过程,伴随DNA早期降解、染色质浓缩、细胞缩小和碎裂。心肌属于终末分化细胞,针对各种应激能够产生一定重塑适应,例如在缺血再灌注、心脏衰竭、衰老情况下会大量凋亡[1-3],导致心肌细胞大量流失,因此细胞凋亡可能会使心肌遭

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