Effect and mechanism of Jiming Powder on myocardial fibrosis in mice with myocardial infarction.
10.19540/j.cnki.cjcmm.20230605.401
- Author:
Xin-Yi FAN
1
;
Xiao-Qi WEI
1
;
Yun-Yang ZHANG
1
;
Hai-Yin PU
1
;
Fang-He LI
1
;
Kuo GAO
1
;
Xue YU
1
;
Shu-Zhen GUO
1
Author Information
1. School of Traditional Chinese Medicine, Beijing University of Chinese Medicine Beijing 100029, China.
- Publication Type:Journal Article
- Keywords:
Jiming Powder;
heart failue;
myocardial fibrosis;
myocardial infarction
- MeSH:
Mice;
Animals;
Transforming Growth Factor beta1/metabolism*;
Matrix Metalloproteinase 2/metabolism*;
beta Catenin/metabolism*;
Matrix Metalloproteinase 3/therapeutic use*;
Powders;
Ventricular Remodeling;
Stroke Volume;
Ventricular Function, Left;
Myocardial Infarction/drug therapy*;
Myocardium/pathology*;
Heart Failure/metabolism*;
Collagen/metabolism*;
Creatine Kinase;
Fibrosis
- From:
China Journal of Chinese Materia Medica
2023;48(21):5838-5850
- CountryChina
- Language:Chinese
-
Abstract:
Jiming Powder is a traditional ancient prescription with good therapeutic effect in the treatment of heart failure, but its mechanism lacks further exploration. In this study, a mouse model of coronary artery ligation was used to evaluate the effect and mechanism of Jiming Powder on myocardial fibrosis in mice with myocardial infarction. The study constructed a mouse model of heart failure after myocardial infarction using the method of left anterior descending coronary artery ligation. The efficacy of Jiming Powder was evaluated from multiple angles, including ultrasound imaging, hematoxylin-eosin(HE) staining, Masson staining, Sirius Red staining, and serum myocardial enzyme spectrum detection. Western blot analysis was performed to detect key proteins involved in ventricular remodeling, including transforming growth factor-β1(TGF-β1), α-smooth muscle actin(α-SMA), wingless-type MMTV integration site family member 3a(Wnt3a), β-catenin, matrix metallopeptidase 2(MMP2), matrix metallopeptidase 3(MMP3), TIMP metallopeptidase inhibitor 1(TIMP1), and TIMP metallopeptidase inhibitor 2(TIMP2). The results showed that compared with the model group, the high and low-dose Jiming Powder significantly reduced the left ventricular internal diameter in systole(LVID;s) and diastole(LVID;d), increased the left ventricular ejection fraction(LVEF) and left ventricular fractional shortening(LVFS), effectively improved cardiac function in mice after myocardial infarction, and effectively reduced the levels of myocardial injury markers such as creatine kinase(CK), creatine kinase isoenzyme(CK-MB), and lactic dehydrogenase(LDH), thus protecting ischemic myocardium. HE staining showed that Jiming Powder could attenuate myocardial inflammatory cell infiltration after myocardial infarction. Masson and Sirius Red staining demonstrated that Jiming Powder effectively inhibited myocardial fibrosis, reduced the collagen Ⅰ/Ⅲ ratio in myocardial tissues, and improved collagen remodeling after myocardial infarction. Western blot results showed that Jiming Powder reduced the expression of TGF-β1, α-SMA, Wnt3a, and β-catenin, decreased the levels of MMP2, MMP3, and TIMP2, and increased the level of TIMP1, suggesting its role in inhibiting cardiac fibroblast transformation, reducing extracellular matrix metabolism in myocardial cells, and lowering collagen Ⅰ and α-SMA content, thus exerting an anti-myocardial fibrosis effect after myocardial infarction. This study revealed the role of Jiming Powder in improving ventricular remodeling and treating myocardial infarction, laying the foundation for further research on the pharmacological effect of Jiming Powder.
