孙其龙, 潘珊珊, 黄悦, 王家银, 陆矫. 2018: 运动预适应通过间歇性缺血缺氧诱导细胞自噬参与早期心肌保护的研究. 体育科学, 38(7): 25-32,49. DOI: 10.16469/j.css.201807015
    引用本文: 孙其龙, 潘珊珊, 黄悦, 王家银, 陆矫. 2018: 运动预适应通过间歇性缺血缺氧诱导细胞自噬参与早期心肌保护的研究. 体育科学, 38(7): 25-32,49. DOI: 10.16469/j.css.201807015
    SUN Qi-long, PAN Shan-shan, HUANG Yue, WANG Jia-yin, LU Jiao. 2018: Exercise Preconditioning Induces Cellular Autophagy by Intermittent Ischemia-Hypoxia to Participate in Early Myocardial Protection. China Sport Science, 38(7): 25-32,49. DOI: 10.16469/j.css.201807015
    Citation: SUN Qi-long, PAN Shan-shan, HUANG Yue, WANG Jia-yin, LU Jiao. 2018: Exercise Preconditioning Induces Cellular Autophagy by Intermittent Ischemia-Hypoxia to Participate in Early Myocardial Protection. China Sport Science, 38(7): 25-32,49. DOI: 10.16469/j.css.201807015

    运动预适应通过间歇性缺血缺氧诱导细胞自噬参与早期心肌保护的研究

    Exercise Preconditioning Induces Cellular Autophagy by Intermittent Ischemia-Hypoxia to Participate in Early Myocardial Protection

    • 摘要: 目的:通过分析运动性心肌缺血缺氧与细胞自噬的关系, 检测自噬相关蛋白Beclin1/Bcl-2在早期运动预适应 (EEP) 及保护期的变化, 探讨细胞自噬在EEP心肌保护效应中的作用。方法:SD大鼠随机分为对照组 (C组) 、早期运动预适应组 (EEP组) 、力竭运动组 (EE组) 和早期运动预适应+力竭运动组 (EEP+EE组) 。1) 用化学发光免疫分析法 (CLIA) 检测血浆cTnI含量, 结合HE和HBFP相邻切片染色, 综合评价心肌缺血缺氧的程度, 验证EEP心肌保护效应。2) 用免疫印迹和免疫荧光双标法检测并观察Beclin1/Bcl-2的表达变化和解离程度。3) 通过相关性分析评估运动性缺血缺氧与细胞自噬的关系。结果:1) 与C组相比, EEP组血浆cTnI水平和MOD值均具有升高的趋势 (P>0.05) , 且EE组和EEP+EE组升高具有显著性 (P<0.05) ;与EE组相比, EEP+EE组cTnI水平和MOD值显著降低 (P<0.05) ;与C组相比, 其余各组心肌组织均显示不同程度的缺血缺氧改变, HE染色嗜酸性增强部位与HBFP染色艳红色阳性区域趋近一致。2) 与C组相比, 其余各组Beclin1均显著升高 (P<0.05) , Beclin1/Bcl-2解离程度增加 (P<0.05) , 而Bcl-2并无明显变化;与EE组相比, EEP+EE组Beclin1/Bcl-2共定位程度显著升高 (P<0.05) 。3) 各组IHA和IOD值均与Beclin1/Bcl-2共定位程度呈显著负相关 (P<0.05) 。结论:EP通过间歇性缺血缺氧可以诱导心肌细胞自噬, 细胞自噬参与了EP对运动性心肌损伤的早期保护效应。

       

      Abstract: Objective: By analyzing the relationships between myocardial ischemia-hypoxia and cellular autophagy in exercise, and by detecting changes of autophagy-associated proteins Beclin1/Bcl-2 in early exercise preconditioning (EEP) and in early protective phase, the effects of cellular autophagy on EEP-cardioprotection were discussed. Methods: SD rats were randomly divided into the groups of control (C group) , early exercise preconditioning (EEP group) , exhaustive exercise (EE group) , and early exercise preconditioning+exhaustive exercise (EEP+EE group) . 1) The plasma cTnI contents were detected by chemiluminescence immunoassay (CLIA) method, which were combined with the adjacent slices between HE-staining and HBFP-staining, to comprehensively assess the extents of myocardial ischemia-hypoxia, and to verify the EEP-cardioprotection. 2) The expressional changes and the dissociated degrees in Beclin1/Bcl-2 were detected by immune-blotting, and were observed by double-labeling immunofluorescence, respectively. 3) The relationships between exercise-induced hypoxia-ischemia and cellular autophagy were assessed by the correlational analysis. Results: 1) Compared with the C group, the plasma cTnI levels and the MOD values in the EEP group to both have increasing tendencies (P>0.05) , and these in the EE group and in the EEP+EE group to were both significant increase (P<0.05) . Compared with the EE group, the plasma cTnI levels and the MOD values in the EEP group to were both significant decrease (P<0.05) . Compared with the C group, all other groups to represent ischemia-hypoxia changes in different degree, which were as the acidophilyenhanced positions in HE-staining approaching to the positive areas of crimson in HBFP-staining. 2) Compared with the C group, all other groups to have significantly increased Beclin1 levels (P<0.05) , and to have increased extents of Beclin1/Bcl-2 dissociations (P<0.05) , but which were without any changes in Bcl-2 levels. Compared with the EE group, the extents of Beclin1/Bcl-2 co-localization were significant increase (P<0.05) . All groups represented with significantly negative correlations between the Beclin1/Bcl-2 co-localization and the ischemia-hypoxia areas, and the IOD values respectively. Conclusion: EP can induces autophagy in cardiomyocytes by intermittent ischemiahypoxia, in which the cellular autophagy participates in the early myocardial protection against the exercise-induced myocardial injury.

       

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