Mechanism of Yangxin Decoction in treating chronic heart failure based on network pharmacology and experimental verification
- VernacularTitle:基于网络药理学与实验验证探讨养心汤治疗慢性心衰大鼠的作用机制
- Author:
Jing-jing CHEN
1
;
Ya-bin ZHOU
;
Yue HE
;
Chao HUANG
;
Wen-feng ZHANG
Author Information
- Publication Type:Journal Article
- Keywords: Yangxin decoction; chronic heart failure; network pharmacology; NLRP3 signaling pathway; in-flammation; experiment; NF-κB
- From: Chinese Pharmacological Bulletin 2025;41(5):942-950
- CountryChina
- Language:Chinese
- Abstract: Aim To explore the mechanism of Yangxin decoction in the treatment of chronic heart failure(CHF)based on network pharmacology and animal ex-periments.Methods The database was used to screen Yangxin decoction,a network of"drug-compo-nent-disease-target"was established,and the obtained targets were enriched and analyzed.The CHF model of rats was replicated by abdominal aortic ligation.After the administration,the general condition,body weight and heart weight of the rats were observed,and the he-modynamic changes,echocardiography indicators and left ventricular mass index were measured.HE staining was used to observe the morphological changes of myo-cardial tissue.Serum IL-1 β,IL-18,TNF-α and BNP were detected by ELISA.The expressions of NLRP3,caspase-1,ASC and NF-κB p65 proteinswere detected by Western blot.Results Enrichment analysis showed that the potential regulatory pathways of Yangx-in decoction in the treatment of CHF involved NOD-like signaling pathway,NF-κB signaling pathway,etc.The results of animal experiments showed that the body weight,left ventricular diastolic diameter and left ven-tricular systolic diameter of the rats in the administra-tion group decreased(P＜0.05),the left ventricular mass index,ejection fraction and short axis narrowing rate increased(P＜0.05),the pathological morphology of myocardial tissue was reduced,and the levels of IL-1 β,IL-18,TNF-α,BNP,NLRP3,caspase-1,ASC and NF-κB p65 decreased(P＜0.05).Conclusions The mechanism of Yangxin decoction in the treatment of CHF rats may be related to inhibiting the activation of NLRP3 inflammasome signaling pathway and reduc-ing the inflammatory response.
