摘要
目的:本文考察游泳训练对小鼠心肌miR-499和相关蛋白的影响,探讨运动干预心肌凋亡的机制。方法:雄性C57BL/6小鼠随机分为3组(n=14):安静组(SE组)、运动训练1组(ET1组)、运动训练2组(ET2)。SE组不运动,ET1组进行8周游泳训练;ET2组在ET1组负荷基础上增加,前5周与ET1相同,后3周每天2次。TUNEL检测心肌凋亡,RT-PCR和Western blot测定miR-499和蛋白。结果:相比SE组,ET1组心肌凋亡指数(AI)、miR-499、Ca N蛋白表达及活性、Drp-1表达均无显著性改变(P>0.05);相比SE组,ET2组AI显著性下降(P<0.01),miR-499表达显著性升高(P<0.05),Drp-1蛋白表达显著性下降(P<0.01),但Ca N蛋白表达及活性无显著改变(P>0.05)。结论:游泳训练能降低心肌凋亡水平,Drp-1表达下降是凋亡率下降的部分机制,但本研究上游Ca N不参与运动调节心肌凋亡的信号。
Objective： To detect the levels of miR-499 and relative proteins in hearts of mice after exercise training, and investigate the mechanism of exercise-regulative apoptosis. Methods： Male C57BL/6 mice were randomly divided into 3 groups（ n = 14） ： sedentary （SE）, exercise training I（ET1） and exercise training 2（E3E） group. SE did not do any exercise. ET1 performed swimming training for 8 weeks. E12 performed the same work as ET1 until the 5th week. Then, mice trained twice a day until the end of training. TUNEL assay was applied to test myocardial apeptosis, RT-PCR and Western blot were used to detect miR-499 and proteins levels respectively. Results： Compared with SE, stress in EF1 failed to affect apoptotic index （AI） and miR-499-CaN- Drp- 1 pathway （ P 〉 0.05）. In contrast, exercise load in EI2 increased miR-499 level, decreased Drp-1 level and AI with statistical significance respectively（ P 〈 0.05）, but neither CaN expression nor CaN activity was changed significantly（ P 〉 0.05）. Conclusion： Swimming training can inhibit myocardial apoptosis, and the decrease in Drp- 1 may be re- sponsible for the reduced myocardial apoptosis. CaN, the upstream protein, does not participate in exereise-regulative apoptosis.
出处
《中国应用生理学杂志》
CAS
CSCD
2015年第3期259-263,共5页
Chinese Journal of Applied Physiology
基金
唐山师范学院科学研究基金项目(2013D03)
关键词
运动
心肌
线粒体
微小RNA
凋亡
小鼠
exercise
myocardium
mitochondria
microRNAs
apoptosis
mice
