中文摘要：

目的：检测和观察心肌线粒体自噬相关蛋白BNIP3在运动预适应（EP）晚期保护效应中的表达变化,探讨EP晚期保护效应和心肌线粒体自噬的关系。方法：SD大鼠随机分为对照组（C组）、力竭运动组（EE组）、晚期运动预适应组（LEP组）、晚期运动预适应＋力竭运动组（LEP＋EE组）和wortmannin＋晚期运动预适应＋力竭运动组（W＋LEP＋EE组）。在EP动物模型的基础上,用力竭运动致大鼠急性心肌损伤,用血浆c Tn I含量和HBFP染色综合评价心肌损伤和保护的程度,用免疫荧光双标法检测大鼠心肌线粒体BNIP3和TOM20的共定位程度,用免疫印迹法检测大鼠心肌组织线粒体BNIP3和LC3的表达变化。结果：与C组相比,EE组血浆c Tn I和MOD值显著升高,BNIP3转位线粒体程度、BNIP3水平和LC3II/I水平显著升高;LEP组BNIP3转位线粒体程度和BNIP3水平显著升高,血浆c Tn I、MOD值和LC3II/I水平无显著性差异。与EE组相比,LEP＋EE组血浆c Tn I和MOD值显著降低,BNIP3转位线粒体程度、BNIP3水平和LC3II/I水平显著降低。与LEP＋EE组相比,W＋LEP＋EE组血浆c Tn I和MOD值显著升高,BNIP3转位线粒体程度和BNIP3水平显著升高,LC3II/I水平无显著性差异。结论：EP可促使线粒体自噬相关蛋白BNIP3表达升高,在EP晚期心肌保护效应中,BNIP3诱导的线粒体自噬参与了EP对运动性心肌损伤的保护作用。

英文摘要：

Objective： To detect and observe the change of mitophagy related protein Bcl-2 19-kDa interacting protein 3 （BNIP3）expression during late cardioprotection of exercise preconditioning, and to determine the relationship between late cardioprotection of exercise preconditioning and myocardial mitophagy. Methods： SD rats were divided into control group （C）, EE group, LEP group, LEP ＋ EE group, and W＋LEP＋EE group. After establishing of EP animal model, exhaus- tive exercise on treadmill for inducing myocardial injury. Then the level of cTnI and hematoxylin basic fuchsin picric acid （HBFP） staining were used to evaluate the degree of myocardial injury and protection. Double immunofluorescence was used to evaluate the transposition of BNIP3 and TOM20. Western blotting method was used to detect change of BNIP3 and LC3. Results： As com- pared with the group C, the cTnI level in plasma and mean optical density （MOD） increased sig- nificantly, the degree of the transposition of BNIP3 to mitochondria, the level of BNIP3 and LC3II/I increased significantly in group EE; While compared with the group C, there was no sig- nificant difference in the cTnI level, MOD and the level of LC3IUI in group LEP, but the degree of the transposition of BNIP3 to mitochondria and the level of BNIP3 increased significantly. As compared with the group EE, the cTnI level in plasma and MOD decreased significantly, the de- gree of the transposition of BNIP3 to mitochondria, the level of BNIP3 and LC3II/I decreased sig- nificantly in group LEP＋EE. As compared with the group LEP＋EE, the cTnI level in plasma and MOD increased significantly, the degree of the transposition of BNIP3 to mitochondria and the level of BNIP3 increased significantly in group W＋LEP＋EE. But there was no significant differ- ence in the level of LC3IUI in group W＋LEP＋EE. Conclusion： Exercise preconditioning can in- duce mitophagy related protein BNIP3 to increase expression, and the mitophagy induced by BNIP3 participated in late cardiop