Moreover, this result was further supported by biochemical and gene expression analyses, as markers such as hydroxyproline content, expression of Tgf-β, α-Sma and Col1a1 in the livers of DA-treated mice were significantly decreased compared to those in CMC-treated BDL mouse livers (Figure 5), suggesting that DA attenuated liver fibrosis and that this effect was companied by suppressed activation of HSCs. Here, TGFB1 is linked to Hepatic fibrosis.