Quercetin improves heart failure by inhibiting cardiomyocyte apoptosis via suppressing the MAPK signaling pathway.
10.12122/j.issn.1673-4254.2025.01.22
- Author:
Xiupeng LONG
1
;
Shun TAO
1
;
Shen YANG
1
;
Suyun LI
1
;
Libing RAO
1
;
Li LI
1
;
Zhe ZHANG
2
Author Information
1. School of Medicine, Hunan University of Medicine, Huaihua 418000, China.
2. Department of Cardiology, Sanya Central Hospital, Sanya 572000, China.
- Publication Type:Journal Article
- Keywords:
MAPK;
heart failure;
isoproterenol;
network pharmacology;
quercetin
- MeSH:
Quercetin/pharmacology*;
Myocytes, Cardiac/drug effects*;
Heart Failure/metabolism*;
Apoptosis/drug effects*;
MAP Kinase Signaling System/drug effects*;
Rats;
Animals;
Isoproterenol
- From:
Journal of Southern Medical University
2025;45(1):187-196
- CountryChina
- Language:English
-
Abstract:
OBJECTIVES:To explore the mechanism that mediate the therapeutic effect of quercetin on heart failure.
METHODS:We searched the TCMSP and Swiss ADME databases for the therapeutic targets of quercetin and retrieved heart failure targets from the Genecards and OMIM databases. The intersecting targets were analyzed with GO and KEGG pathway analysis using DAVID database, and the key genes were identified via PPI analysis. Molecular docking between the core targets and quercetin was performed using PyMOL and AutoDock Tools. In a heart failure model established in H9C2 cardiomyocytes by treatment with isoproterenol, the effect of quercetin on the expressions of the MAPK signaling pathway was tested.
RESULTS:A total of 60 intersecting targets were identified. Enrichment analysis revealed that quercetin may inhibit heart failure through the MAPK signaling pathway. The core genes, including AMPK3 and BCL-2, were identified as potential key regulators in quercetin-mediated improvement of heart failure. Cellular experiments demonstrated that quercetin significantly reduced isoproterenol-induced apoptosis of cardiomyocytes in a dose-dependent manner and obviously decreased the Bax/Bcl-2 ratio and the expression levels of caspase-3, ERK and p38 in the cells.
CONCLUSIONS:Quercetin improves heart failure possibly by inhibiting cardiomyocyte apoptosis through the MAPK signaling pathway.
