Impact of Qiangxin Tang on Myocardial Fibrosis in Rats with Chronic Heart Failure Mediated by BNIP3/NIX/FUNDC1 Pathway and Myo-cardial Mitochondrial Autophagy
10.11969/j.issn.1673-548X.2025.01.009
- VernacularTitle:强心汤通过BNIP3/NIX/FUNDC1途径介导心肌线粒体自噬对慢性心力衰竭大鼠心肌纤维化的影响
- Author:
Yan PANG
1
;
Jianqi LU
;
Jiayong CHEN
Author Information
1. 530000 南宁,广西中医药大学;530022 南宁,广西中医药大学第一附属医院
- Publication Type:Journal Article
- Keywords:
Chronic heart failure;
Qiangxin Tang;
Mitochondrial autophagy;
BNIP3/NIX/FUNDC1;
Myocardial fibrosis
- From:
Journal of Medical Research
2025;54(1):43-47
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the impact of Qiangxin Tang on myocardial fibrosis in rats with chronic heart failure by mediating myocardial mitochondrial autophagy through the Bcl-2/adenovirus E1B 19kDa interacting protein 3/NIP3 like protein X and FUN14domain-containing protein 1.Methods Forty Sprague Dawley rats were divided into five groups randomly by the random number table:sham operation group,model group,Qiangxin Tang group,Captopril group,and Qiangxin Tang+Captopril group,with a total of eight rats in each group.Only the sham operation group threaded without ligating the left coronary artery of the heart.In all the other groups,CHF rat models were established after myocardial infarction by ligating the left coronary artery of the heart.From the day after successful modeling,each group was given corresponding drugs by gavage,and the left ventricular myocardial tissue of each group was de-tected.Western blot was used to detect the expression of NIX,BNIP3,and FUNDC1 proteins in each group.ELISA was used to detect brain natriuretic peptide and cardiac troponin T level.Mitochondrial morphology was observed under transmission electron microscopy.Masson staining was used to observe left ventricular myocardial fibrosis.Results Compared with the sham surgery group,the expression of NIX,BNIP3 and FUNDC1 proteins in the model group was significantly reduced,while the levels of BNP and cTnT were significantly increased(P＜0.05).The left ventricular myocardial tissue showed significant fibrosisand mitochondrial swelling.Compared with the model group,the expression of NIX,BNIP3,and FUNDC1 proteins was significantly increased in Qiangxin Tang group and Captopril group,while the levels of BNP and cTnT were significantly decreased(P＜0.05).The left ventricular myocardial tissue fibrosis was sig-nificantly reduced,and the mitochondrial morphology was mildly altered.Compared with Qiangxin Tang group and Captopril group,the Qiangxin Tang+Captopril group showed significant improvement in the above indicators,and there was no significant difference in the in-dicators between Qiangxin Tang group and Captopril group.Conclusion Qiangxin Tang may promote mitochondrial autophagy and ensure the morphology and function of mitochondrial by upregulating the expression of NIX,BNIP3 and FUNDC1,thereby reducing myocardial injury and fibrosis.In addition,the combination of Qiangxin Tang and Captopril has a better therapeutic effect on CHF.
