Objective  To observe the epithelial-mesenchymal transition (EMT）of human intrahepatic biliary epithelial cells (HIBEpiC) and to study its role in bile duct fibrosis and its molecular mechanism.    Methods  Expressions of E-cadherin

S100A4

α-SMA

and EMT signal-related TGF-β1 in HIBEpiC were detected by RT-PCR and Western blotting 48 and 72 h after treatment of HIBEpiC with lipopolysaccharide (LPS). The effect of TGF-β1 was blocked with paclitaxel and siRNA smad2/3. The role of TGF-β1/ smad2/3 signal pathway in the occurrence of EMT in HIBEpiC was studied.    Results  The expression of TGF-β1 mRNA reached its  peak and began to decrease 48 and 72 h

respectively

after treatment of HIBEpiC with LPS

and still maintained a rather high level (P0.01

0.05). The expression level of EMT marker

E-cadherin mRNA and TGF-β1 decreased with the prolongation of culture time ( P0.01) while the expression of S100A4

α-SMA mRNA and TGF-β1 significantly increased （P0.01，0.05）

suggesting that paclitaxel can down-regulate the LPS-induced expression of TGF-β1

Smad2 and Smad3 mRNA. siRNA could also down-regulate the LPS-induced expression of Smad2/3 mRNA

S100A4

α-SMA and TGF-β1 while up-regulate the expression of E-cadherin and TGF-β1 in HIBEpiC (P0.01)

indicating that EMT can be reversed.    Conclusion  LPS can induce expression of TGF-β1 in HIBEpiC

resulting in EMT in biliary epithelial cells

and reverse EMT by inhibiting TGF-β1 or Smad2/3

which may be a potential target for the prevention and treatment of  biliary fibrosis.