Daidzein stimulates collagen synthesis by activating the TGF-β/smad signal pathway

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Abstract

Background/Objectives:

The objective of this study was to investigate the effects of daidzein on collagen metabolism and its underlying mechanism in cultured skin fibroblast and nude mouse skin.

Methods:

Skin fibroblasts were exposed to different concentrations of daidzein (0.5–50 μg/mL) for 24 h or 48 h, respectively. Female nude mice were treated topically with 200 μg/mL daidzein once a day for 6 weeks. Cell viability and cell cycle were determined by MTT and flow cytometer. The transcriptional activity of collagen type I was evaluated and the expression of procollagen, matrix metalloproteinase-1 (MMP1) and MMP2 were measured by real-time polymerase chain reaction. A Western blot analysis was applied to detect the levels of phosphorylated-Smad2 and Smad3.

Results:

In the daidzein-treated cells the expression of type I procollagen increased markedly while the expressions of MMP1, and MMP2 was significantly inhibited. Additionally, the mouse skin showed more collagen deposition after daidzein treatment. The levels of transforming growth factor (TGF)-β, phosphorylated-smad2 and smad3 were also higher in the daidzein treated skin fibroblasts than in the controls.

Conclusions:

The results showed that daidzein treatment can increase skin collagen synthesis and inhibit collagen degradation in vitro and in vivo. It seems that TGF-β/smad signalling pathways play an important role in daidzein-induced collagen accumulation.

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