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

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-beta 1 and TGF beta RI levels were gradually decreased by daidzein in a dose-dependent manner. In the current study, we show that daidzein significantly inhibited TGF-beta 1-induced mRNA and protein expression of alpha-SMA, collagen I, and collagen III. Accordingly, immunofluorescence staining of alpha-SMA was performed. Daidzein also inhibited TGF beta 1-induced cardiac fibroblast proliferation and migration. Mechanistically, daidzein inhibited the TGF-beta/SMAD signaling pathway induced by TGF-beta 1 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-beta 1-induced cardiac fibroblast activation by partially regulating the TGF-beta 1/SMAD2/3 signaling pathway.

Automated summary

This study reveals that daidzein has an anti-fibrotic effect in myocardial fibrosis by reducing the activation of cardiac fibroblasts induced by TGF-beta 1, partially through regulating the TGF-beta 1/SMAD2/3 signaling pathway.