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. This evidence concerns the gene COL1A1 and Hepatic fibrosis.