| Based on the predecessors,this study established a model of exercise-induced myocardial ischemia and myocardial ischemia-reperfusion injury after moderate-intensity training in rats.The autophagy inhibitor 3-MA was used to control the autophagy of rat myocardium.And analysis of autophagy regulation is involved in exercise preconditioning myocardial protection.Objective: To establish a RAT model of exercise-induced myocardial ischemia and myocardial ischemia-reperfusion injury after moderate intensity training in rats based on previous studies,used autophagy inhibitor 3-MA for the regulation of rat myocardial autophagy,and analyzed whether autophagy had an effect on exercise-induced myocardial injury.Methods: Forty-eight healthy male SD rats(SPF grade)aged 8 weeks were provided by Hunan Slake Jingda Laboratory Animal Co.,Ltd.They were divided into six groups: exercise-induced myocardial ischemia quiet modeling group(Q1),exercise-induced myocardial ischemia training non-inhibition group(A),exercise-induced myocardial ischemia training 3-MA inhibition group(B),myocardial ischemia reperfusion quiet modeling group(Q2),myocardial ischemia reperfusion training non-inhibition group(C),myocardial ischemia reperfusion training 3-MA inhibition group(D),eight rats in each group.With reference to the Bedford standard and the exercise protocol established by Ding Shuzhe et al.,treadmill training was performed on rats,in which Q1 and Q2 groups were the quiet control group without training(direct modeling),and the rest groups were trained for 5 days per week with 2 days rest.Electrocardiogram observation,fluorescence quantitative PCR detection of autophagy-related gene expression changes,and Western blotting detection of autophagy-related protein expression changes were performed for each rat.Study Results: 1.The results of ECG showed ST segment depression(J point)in Q1,A and B groups.The ST segment depression(J point)in group AB was significantly higher than that in group Q1(p < 0.01).The ST segment depression(J point)in group B was significantly higher than that in group A(p < 0.01).In Q2,C and D groups,ST segment elevation occurred during the ischemic phase and decreased during the reperfusion phase.There were no significant differences between the three groups in the preoperative period.During the ischemic period,the amplitude of ST segment elevation in groups C and D was significantly lower than that in group Q2(p < 0.01),and the degree of ST segment elevation in groups D and C was significantly increased(p < 0.01).In the reperfusion period,the amplitude of ST segment elevation in groups C and D was significantly lower than that in group Q2(p < 0.01),and the degree of ST segment elevation in groups D and C was significantly increased(p < 0.01).2.The results of serum CK-MB in rat heart showed that the content of serum CK-MB was significantly lower in group A and B compared with group Q1(p < 0.01).The level of CK-MB in group A was significantly lower than that in group B(p < 0.01).Compared with Q2 group,the content of CK-MB in serum was significantly decreased in C and D groups(p < 0.01),indicating that the level of myocardial injury in AB group was lower than that in Q2 group after 8 weeks training.The level of CK-MB in group C was significantly lower than that in group B(p < 0.01).3.Fluorescence quantitative PCR detection of autophagy-related genes LC3-1,LC3-2,Beclin1 expression results showed that the expression level of autophagy-related genes LC3-1 in group A and B was significantly lower(p < 0.01)than that in the group of quiet rats(Q1);in group C and D was significantly lower(p < 0.01)than that in the group of quiet rats(Q2).The expression level of autophagy-related genes LC3-2 and Beclin1 was significantly higher(p < 0.01)than that in the quiet rats.In the exercise-induced myocardial ischemia group,the expression level of the autophagy-related gene LC3-1 in the autophagy inhibitor 3-MA intervention group(group B)was significantly lower(P < 0.01)than that in the non-inhibition group(group A)rats;the expression level of the autophagy-related genes LC3-2 and Beclin1 was significantly higher(P < 0.01)than that in the non-inhibition group(group A)rats.In the myocardial ischemia-reperfusion group,the expression level of the autophagy-related gene LC3-1 in the autophagy inhibitor 3-MA intervention group(group D)was significantly lower(P < 0.01)than that in the non-inhibition group(group C)rats;the expression level of the autophagy-related genes LC3-2 and Beclin1 was significantly higher(P < 0.01)than that in the non-inhibition group(group C)rats.4.The results of autophagy-related protein expression detected by Western blotting showed that the expression level of autophagy-related protein LC3-1 in group A and B was significantly lower(p < 0.01)than that in the group of quiet rats(Q1);in group C and D was significantly lower(p < 0.01)than that in the group of quiet rats(Q2).The expression level of autophagy-related protein Beclin1 was significantly higher(P < 0.01)than that in quiet rats.In the exercise-induced myocardial ischemia group,the expression level of autophagy-related protein LC3-1 in the autophagy inhibitor 3-MA intervention group(group B)was significantly lower(P < 0.01)than that in the non-inhibition group(group A)rats;the expression level of Beclin1 was significantly higher(P < 0.01)than that in the non-inhibition group(group A)rats.In the myocardial ischemia-reperfusion group,the expression level of autophagy-related protein LC3-1 in the autophagy inhibitor 3-MA intervention group(group D)was significantly lower(P < 0.01)than that in the non-inhibition group(group C)rats;the expression level of Beclin1 was significantly higher(P < 0.01)than that in the non-inhibition group(group C)rats.CONCLUSION: Exercise of appropriate intensity can reduce the injury of heart in exercise-induced myocardial ischemia and myocardial ischemia-reperfusion,cause the adaptive upregulation of autophagy level of cardiomyocytes,promote the enhancement of metabolic capacity and contractile function of cardiomyocytes,and thus play a certain protective role in exercise-induced myocardial ischemia and myocardial ischemia-reperfusion injury. |
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