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.
Keywords: Cardiac fibroblasts; Daidzein; Myocardial fibrosis; TGF-β1; TGF-β1/SMAD2/3 signaling pathway.
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