有氧间歇训练对心肌梗死大鼠心肌细胞增殖作用及相关机制.docVIP

有氧间歇训练对心肌梗死大鼠心肌细胞增殖作用及相关机制 江红轲作者简介： 作者简介：江红轲(1976-),男，讲师，在读医学博士，研究方向：运动与心血管病理药理学；电子信箱:jianghk88@126.com; 联系方式 （南阳理工学院体育教学部，河南 南阳 473003） 摘 要:目的: 通过建立SD大鼠心肌梗死动物模型，观察间歇训练对心梗大鼠心肌细胞的增殖作用，并探讨其内在影响机制。方法:实验材料为成年雄性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13只。术后自然恢复1周后进行间歇训练，共计8周。形态学检测大鼠心肌梗死区边缘增殖细胞核抗原PCNA、Ki-67及BrdU水平；分子水平测定胰岛素样生长因子受体（IGF-R）1,2, PI3K-AKt生存通路及mTOR-p70S6K信号系统活性。结果:形态学结果提示，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表达水平。蛋白检测表明，心梗组大鼠细胞膜IGF-R1水平显著性降低（P0.01），PI3K-AKt-mTOR-p70S6K信号系统活显著性降低（P 0.01）; 相对地， 间歇训练上调IGF-R1水平（P 0.05），有效对抗心梗造成的上述信号通路失活作用（P 0.05）。但无论是心梗和运动对IGF-R2水平均无显著性影响（P0.05）。结论：心梗可引起梗死边缘区细胞代偿性增加，其增加作用与IGF-R1介导的增殖通路呈负相关。间歇训练引起的细胞增殖作用可能与上述通路激活作用相关。 关键词: 心肌梗死，细胞增殖，间歇训练，生存通路，哺乳动物雷帕霉素靶蛋白，核糖体蛋白S6激酶 Proliferation Effect-mediated by Aerobic Interval Training on Myocardial Infarction Rats and its partial Involved Mechanism Hong ke Jiang (Department of Nanyang Institute of Abstract: objective: Through establishment of myocardial infarction animal models in SD rats and observation of interval training on the role of myocardial cell proliferation, the aim of this manuscript is to explore the internal impact mechanism of exercise on myocardial proliferation. Methods: 40 adult male SD rats were used for 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 = 13 in each group. After 1 week natural recovery, rats in AIT group performed interval training and lasted for 8 weeks. Morphological demonstrated that myocardial infarction proliferating cell nuclear antigen PCNA, Ki-67 and BrdU levels; molecular level measured insulin-like growth factor receptor (IGF-R) 1,2, PI3K-AKt survival pathway and the mTOR-p70S6K signaling system activity as well. Results: The morphological results suggest that cell proliferation in normal myocardium is rare; myocardial infarction can cause infarcti