Effects and mechanism of Qiangxin decoction on mitochondrion of rats with chronic heart failure
- VernacularTitle:强心汤对慢性心力衰竭大鼠线粒体的影响及机制
- Author:
Meiling MAO
1
;
Jianqi LU
2
;
Zhide ZHU
2
;
Yan PANG
2
;
Liyu XIE
1
;
Jiayong CHEN
1
;
Xinyu WU
1
;
Xiang XIAO
1
;
Junshen LU
3
;
Weiqi SHI
1
Author Information
1. First Clinical School，Guangxi University of Chinese Medicine，Nanning 530299，China
2. Cardiovascular Department，the First Affiliated Hospital of Guangxi University of Chinese Medicine，Nanning 530023，China
3. Affiliated School of Traditional Chinese Medicine，Guangxi University of Chinese Medicine，Nanning 530001，China
- Publication Type:Journal Article
- Keywords:
Qiangxin decoction;
chronic heart failure;
mitochondrion;
energy metabolism;
fibrosis;
PA/Mfn/CL signaling
- From:
China Pharmacy
2025;36(2):160-165
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the effects and potential mechanism of Qiangxin decoction on mitochondrion of rats with chronic heart failure （CHF）. METHODS The CHF model was established by ligating the left anterior descending branch of the coronary artery. Modeled rats were divided into model group， Qiangxin decoction low-dose and high-dose groups （12.25， 24.50 g/kg， calculated by crude drug）， and chemical medicine group （Sacubitril valsartan sodium tablets， 10.42 mg/kg）， with 10 rats in each group； control group was set up without treatment. Each group of rats was orally administered with the corresponding medication or normal saline twice a day for 28 consecutive days. After the last medication， the contents of N-terminal pro-brain natriuretic peptide （NT-proBNP） and adenosine triphosphate （ATP） in serum and phosphatidic acid （PA） and cardiolipin （CL） in myocardial tissue were all detected； the pathological damage and collagen fibrosis of rat myocardial tissue were observed； the apoptosis of myocardial cells was determined； the ultrastructure of myocardial tissue was observed； the protein expressions of mitofusin 1 （Mfn1）， Mfn2， optic atrophy protein 1 （OPA1） and dynamin-related protein 1 （Drp1） were all detected in myocardial tissue. RESULTS Compared with control group，the serum content of NT-proBNP， apoptotic rate of myocardial cells， and relative expressions of S-OPA1 and Drp1 proteins were all increased significantly； serum content of ATP，contents of PA and CL， and relative expressions of Mfn1， Mfn2 and L-OPA1 proteins were all significantly reduced （P＜0.05）. There were abnormal membrane tissue structure in various layers of myocardial tissue， degeneration and necrosis of myocardial cells， and severe fibrosis； the mitochondria were swollen， with reduced or absent cristae， and uneven matrix density. After intervention with Qiangxin decoction， the levels of the aforementioned quantitative indicators in serum and myocardial tissue of rats （excluding CL content in the Qiangxin decoction low- dose group） were significantly reversed （P＜0.05）； the pathological damage of myocardial tissue had significantly improved， fibrosis had significantly reduced， mitochondrial morphology tended to be normal， cristae had increased， and matrix density was uniform. CONCLUSIONS Qiangxin decoction can regulate myocardial mitochondrial function and structural integrity of CHF rats， thereby improving myocardial energy metabolism and antagonizing myocardial fibrosis， the mechanism of which may be associated with activating PA/Mfn/CL signaling pathway.
