Molecular Mechanism Analysis of Dengzhan Shengmai Capsules Against Myocardial Fibrosis After Myocardial Infarction Based on Network Robustness Algorithm
10.13422/j.cnki.syfjx.20260108
- VernacularTitle:基于网络稳健性探讨灯盏生脉胶囊对心梗后心肌纤维化大鼠的调控作用
- Author:
Feifei OU
1
;
Bo ZHANG
2
;
Fuzhu PAN
2
;
Junying WEI
2
;
Hongwei WU
2
;
Minghua XIAN
1
;
Jing XU
2
Author Information
1. School of Traditional Chinese Medicine（TCM）， Guangdong Pharmaceutical University， Guangzhou 510006， China
2. Institute of Chinese Materia Medica， China Academy of Chinese Medical Sciences， Beijing 100700， China
- Publication Type:Journal Article
- Keywords:
myocardial infarction;
Dengzhan Shengmai capsules;
myocardial fibrosis;
network robustness;
neutrophil
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(19):164-173
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the potential therapeutic effects of Dengzhan Shengmai capsules （DZSM） on myocardial fibrosis after myocardial infarction and decipher the underlying molecular mechanisms by virtue of network robustness algorithm. MethodsA rat model of myocardial infarction was established by ligating the left anterior descending coronary artery. Successfully modeled Sprague-Dawley rats were randomly allocated into a model group， an enalapril group（3.15 mg·kg-1）， and high- and low-dose DZSM groups（226.8，113.4 mg·kg-1）. In addition， a sham group was set up. After four consecutive weeks of intervention， the cardiac function was assessed via echocardiography， and myocardial collagen deposition was observed through Sirius red staining. The key regulatory pathways of DZSM were analyzed by the network robustness algorithm. Enzyme-linked immunosorbent assay （ELISA） and immunofluorescence assay were employed to validate the mechanisms. ResultsCompared with the sham group， the model group exhibited decreased left ventricular ejection fraction （LVEF%） and fractional shortening （FS%） （P<0.01） and increased myocardial collagen volume fraction （CVF%） （P<0.01）. Compared with the model group， high-dose DZSM and enalapril improved LVEF% and FS% （P<0.01）. Both high- and low-dose DZSM reduced the CVF% （P<0.05， P<0.05，）. Network analysis indicated that DZSM exerted its effects by regulating neutrophil infiltration and related inflammatory pathways. Experimental validation showed that DZSM significantly reduced the protein levels of nuclear factor （NF）-κB， Janus kinase 2 （JAK2）， and signal transduction activator and transducer 3 （STAT3） in the cardiac tissue， as well as the levels of chemokine （C-X-C motif） ligand 1 （CXCL1）， interleukin （IL）-1β， neutrophil elastase-DNA complex （NE-DNA）， and myeloperoxidase-DNA complex （MPO-DNA） in the plasma. ConclusionDZSM may ameliorate myocardial fibrosis by inhibiting neutrophil infiltration and extracellular trap formation and regulating the NF-κB/JAK2/STAT3 signaling pathway.
