Zhao Yong-Cai, Fu Jin-Mei, Gao Bing-Hong
Shanghai University of Sport, Shanghai 200438.
Institute for Sports Science of Jiangxi Province, Nanchang 330006, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2018 Jan 8;34(1):93-96. doi: 10.12047/j.cjap.5502.2018.023.
To detect the levels of miR-1, miR-21 and their targeted proteins in hearts of mice after different exercise training, and discuss potential molecular mechanism.
Male C57BL/6 mice were randomly divided to 3 groups:sedentary (SE), exercise training 1(ET1) and exercise training 2 (ET2). SE did not do any exercise; ET1 undertook swimming training for 8 weeks, once a day, 5 days/week. Swimming 30 min in the 1 week, and the duration was increased 10 min per week to 90 min and maintained in the 7 and 8 week. ET2 performed the same work as ET1 and switched to twice a day by the end of the 5th week. TUNEL assay was applied to test myocardial apoptosis. Western blot and RT-PCR were used to detect proteins and miRs levels respectively.
Compared with SE, in ET1, myocardial apoptosis and miR-1 level did not change, but its targeted protein Bcl-2 increased significantly(<0.01). miR-21 and its targeted protein PDCD4 did not change significantly. In ET2, myocardial apoptosis and miR-1 level were decreased significantly(<0.05). Bcl-2 was increased significantly(<0.01). miR-21 also increased significantly (<0.05), but PDCD4 did not decrease significantly.
Exercise training in ET2 other than ET1 could down-regulate myocardial apoptosis. Alterations of miR-1 and Bcl-2 may be responsible for this cardioprotection. PDCD4 is not sensitive to exercise training, it is likely that miR-21 and other targeted proteins participate in exercise-regulative apoptosis.
检测不同运动训练后小鼠心脏中miR-1、miR-21及其靶向蛋白的水平,并探讨其潜在的分子机制。
将雄性C57BL/6小鼠随机分为3组:静息组(SE)、运动训练1组(ET1)和运动训练2组(ET2)。SE组不进行任何运动;ET1组进行8周游泳训练,每天1次,每周5天。第1周游泳30分钟,此后每周游泳时间增加10分钟,直至第7周和第8周达到90分钟并维持。ET2组训练方式与ET1组相同,但在第5周结束时改为每天训练2次。采用TUNEL法检测心肌细胞凋亡情况。分别用蛋白质免疫印迹法和逆转录-聚合酶链反应法检测蛋白和miR水平。
与SE组相比,ET1组心肌细胞凋亡和miR-1水平未发生变化,但其靶向蛋白Bcl-2显著增加(<0.01)。miR-21及其靶向蛋白PDCD4无显著变化。ET2组心肌细胞凋亡和miR-1水平显著降低(<0.05)。Bcl-2显著增加(<0.01)。miR-21也显著增加(<0.05),但PDCD4未显著降低。
ET2组而非ET1组的运动训练可下调心肌细胞凋亡。miR-1和Bcl-2的改变可能是这种心脏保护作用的原因。PDCD4对运动训练不敏感,可能是miR-21和其他靶向蛋白参与了运动调节的细胞凋亡。