有氧间歇训练对心肌梗死大鼠心肌细胞的增殖作用及相关机制  

Proliferation Effect-mediated by Aerobic Interval Training on Myocardial Infarction Rats and its Partial Involved Mechanism

作　　者：江红轲[1,2] 

机构地区：[1]南阳理工学院体育教学部,河南南阳473003 [2]西安交通大学医学院药理学系,西安710062

出　　处：《河南师范大学学报（自然科学版）》2012年第4期107-112,共6页Journal of Henan Normal University(Natural Science Edition)

基　　金：河南省科技攻关项目.(112102310694)

摘　　要：目的:通过建立SD大鼠心肌梗死模型,观察间歇训练对心梗大鼠心肌细胞的增殖作用并探讨其内在作用机制.方法:成年雄性SD大鼠40只,造模后,随机分为3组:假心梗组(CON);心梗组(MI);心梗+间歇训练组(MI+AIT),每组12只.间歇训练共计8周.结果:免疫组化结果提示,正常心肌组织鲜见细胞增殖现象;心肌梗死可造成梗死边缘区细胞代偿性增加;间歇训练可显著性增加细胞增殖核抗原PCNA,BrdU和ki-67的表达水平.另外,心梗还可引起细胞增殖核抗原调节蛋白p70S6K及其上游调节蛋白mTOR显著性降低(P<0.05);而mTOR的上游调节蛋白PI3K,Akt也具有相似的变化趋势.相对地,间歇训练可增加心肌细胞膜IGF-R1水平(非IGF-R2),上调PI3K-AKt-mTOR信号通路活性,增加p70S6K磷酸化水平(P<0.05).结论:间歇训练介导的细胞增殖作用与其上调IGF-R1表达水平,激活细胞PI3K-Akt介导的增殖通路相关.Objective： Through establishment of myocardial infarction animal models in SD rats and observation of inter- val training on the role of myocardial cell proliferation. Methods： 40 adult male SD rats were used as experimental material. After the model were produced, samples randomly divided into 3 groups.. Sham MI group （CON） ; Myocardial infarction group （MI）; Myocardial infarction ＋ interval training group （MI＋AIT）, n = 12 in each group. Interval training lasted for 8 weeks. Results： Immunohistochemical results suggest that cell proliferation in normal myocardium is rare; myocardial infarction can cause infarction compensatory increase in＇the marginal zone cells; Interval training significantly increased the expression level of proliferating cell nuclear antigen of PCNA, BrdU and Ki-67. Myocardial infarction can significantly decrease the prolif- erating cell nuclear antigen regulatory proteins p70S6K and its upstream regulatory protein mTOR （P〈0.05）, PI3K-Akt signaling-one regulation unit for roTOR has a similar trend. Comparatively, Interval training activates the PI3K-Akt-of mTOR-of pTOS6K signal pathway via upregulating IGF-R1 content not IGF-R2 （P〈0.05）. Conclusion： AIT-mediated cell proliferation may be associated with increasing IGF-R1 level and thus further activating of PI3K-AKt signal cascades.

关 键 词：心肌梗死 细胞增殖 间歇训练 哺乳动物雷帕霉素靶蛋白 核糖体蛋白S6激酶 

分 类 号：G807.4[文化科学—体育训练]