Changes Of Myocardial Mitophagy Related Protein BNIP3 During Late Cardioprotection Of Exercise Preconditioning

Objective:Exercise preconditioning(EP)can induce endogenous cardioprotection by exercise,and its mechanism involves many aspects.Mitochondria is an important participant in cardioprotection of EP.The upregulation of mitophagy can timely eliminate damaged mitochondria,which is good for maintaining cell survival.Bcl-2 19-kDa interacting protein 3(BNIP3)has the function of regulating autophagy,and can participate in myocardial mitophagy with the damaged mitochondria.In this study,to detect and observe the change of mitophagy related protein 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,exhaustive exercise on treadmill for inducing myocardial injury.Then the level of cTnl and hematoxylin basic fuchsin picric acid(HBFP)staining were evaluated the degree of myocardial injury and protection.Double immunofluorescence was evaluated the transposition of BNIP3 and TOM20.Western blotting method was used to detect change of BNIP3 and LC3.Results:As compared with the group C,the cTnl level in plasma and mean optical density(MOD)increased significantly,the degree of the transposition of BNIP3 to mitochondria,the level of BNIP3 and LC3Ⅱ/Iincreased significantly in group EE;While compared with the group C,there was no significant difference in the cTnl level,MOD and the level of LC3II/I 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 cTnl level in plasma and MOD decreased significantly,the degree of the transposition of BNIP3 to mitochondria,the level of BNIP3 and LC3II/I decreased significantly 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 difference in the level of LC3II/I in group W+LEP+EE.Conclusion:Late exercise preconditioning can attenuate high-intensity exhaustive exercise-induced myocardial injury.Autophagy can participate in late cardioprotection of EP.High-intensity exhaustive exercise and late exercise preconditioning can induce BNIP3 to increase expression,and to participate in myocardial mitophagy.The mitophagy induced by BNIP3 participated in late cardioprotection of exercise-induced myocardial injury during late exercise preconditioning.