ReferenceID 5076

Daidzein suppresses TGF-β1-induced cardiac fibroblast activation via the TGF-β1/SMAD2/3 signaling pathway

Eur J Pharmacol

Myocardial fibrosis is a concomitant bioprocess associated with many cardiovascular diseases (CVDs). Daidzein is an isoflavone that has been used for the treatment of CVDs. This study aimed to reveal its role in myocardi

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Reference Id
5076
Evidence Id
21666
Core Evidence Id
21666
Source Reference Id
3432
Herb2 Reference Id
HBREF004229
Subject Paper Key
HBIN022577_35151651
Pubmed Id
35151651
Doi
10.1016/j.ejphar.2022.174805
Paper Title
Daidzein suppresses TGF-β1-induced cardiac fibroblast activation via the TGF-β1/SMAD2/3 signaling pathway
Paper Abstract
Myocardial fibrosis is a concomitant bioprocess associated with many cardiovascular diseases (CVDs). Daidzein is an isoflavone that has been used for the treatment of CVDs. This study aimed to reveal its role in myocardial fibrosis. Our results indicate that daidzein had a nontoxic effect on cardiac fibroblasts and that TGF-β1 and TGFβRI levels were gradually decreased by daidzein in a dose-dependent manner. In the current study, we show that daidzein significantly inhibited TGF-β1-induced mRNA and protein expression of α-SMA, collagen I, and collagen III. Accordingly, immunofluorescence staining of α-SMA was performed. Daidzein also inhibited TGF-β1-induced cardiac fibroblast proliferation and migration. Mechanistically, daidzein inhibited the TGF-β/SMAD signaling pathway induced by TGF-β1 in cardiac fibroblasts. Additionally, daidzein ameliorated MI-induced cardiac dysfunction and cardiac fibrosis in vivo. Based on these findings, we conclude that daidzein reduces TGF-β1-induced cardiac fibroblast activation by partially regulating the TGF-β1/SMAD2/3 signaling pathway.
Journal
Eur J Pharmacol
Publish Year
2022
Experiment Subject
Experiment Type
Cell Experiment
Phenotype Related
Myocardial Fibrosis; Cardiovascular Diseases; Cardiac Dysfunction; Cvds; Cardiac Fibrosis
Paper Title Cn
Paper Title En
Daidzein suppresses TGF-β1-induced cardiac fibroblast activation via the TGF-β1/SMAD2/3 signaling pathway
Bilingual Status
semi_complete