Study on the mechanism of endurance exercise regulating miR-378 to improve cardiac fibrosis in rats with pressure overload-induced heart failure
10.3969/j.issn.1001-1242.2025.02.003
- VernacularTitle:耐力运动调控miR-378改善压力超负荷型心力衰竭大鼠心脏纤维化的机制研究
- Author:
Siyuan HU
1
;
Xiajun XIONG
;
Senjie ZHONG
Author Information
1. 湖南中医药大学体育艺术学院,湖南省长沙市,410208;武汉体育学院运动医学院
- Publication Type:Journal Article
- Keywords:
endurance exercise;
miR-378;
heart failure;
cardiac fibrosis
- From:
Chinese Journal of Rehabilitation Medicine
2025;40(2):180-187
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the mechanism of exercise on improving cardiac fibrosis in heart failure,and the role of miR-378 in regulating Cardiac fibrosis by endurance exercise.Method:Twenty-four SD rats were selected and used transverse aortic constriction(TAC)to replicate the rat model of heart failure with cardiac fibrosis.They were randomly divided into the sham group,the TAC group and the exercise group.The exercise group performed swimming endurance exercise for 6 weeks.After train-ing,the rats in each group were analyzed by echocardiography and pathological morphology,and the serum NT-proBNP concentration was detected by ELISA.Western Blot and qPCR were used to detect the expression of α-SMA,Col Ⅰ,Col Ⅲ,TGF-β1,miR-378,TGF-β1 mRNA,Col1a1,and Col3a1 in heart tissue.Result:Compared with the sham group,left ventricular ejection fraction(LVEF),left ventricular short-axis shortening(LVFS),and output per beat(SV)were significantly decreased(P＜0.05)in TAC group,and there were no significant differences in left ventricular end-diastolic volume(EDV)and left ventricular end-systolic volume(ESV)(P＞0.05),and the serum NT-proBNP concentration was increased significantly(P＜0.01).Patho-logical staining in TAC group showed that cardiomyocytes were obviously edematous and disorganzied,and col-lagen volume fraction(CVF)was significantly increased(P＜0.05);the expression of fibrosis-related factors α-SMA,Col Ⅰ,Col Ⅲ,TGF-β1,TGF-β1 mRNA,Col1a1 and Col3a1 was significantly up-regulated(P＜0.05),and the expression of miR-378 was significantly down-regulated(P＜0.05).Compared with the TAC group,in the Ex group,LVEF,LVFS,SV increased significantly(P＜0.05),LVIDs,ESV decreased significantly(P＜0.01),NT-proBNP concentration decreased(P＜0.05);CVF decreased significantly(P＜0.05).The expressions of Col Ⅰ,Col Ⅲ,Col1a1 and Col3a1 in heart tissues were significantly reduced(P＜0.05),α-SMA was not significantly different,and the expression of miR-378 increased(P＜0.05).The expression of TGF-β1 and mRNA was reduced(P＜0.05).Conclusion:TAC can better replicate the cardiac fibrosis model of pressure-overload heart failure.Endurance exercise can up-regulate miR-378 expression,which can effectively improve the level of cardiac fibrosis,slow down the degree of heart failure,and restore cardiac function.This mechanism of action may be related to the inhibition of cardiac fibroblast activation by exercise-regulated miR-378.
