Objective To explore the anti hepatic fibrosis effect of dihydroartemisinin in vitro and the possible mechanism. Methods Eight concentration of dihydroartemisinin（50

25

12. 5

6. 25

3. 125

1. 5625

0. 78125 and 0. 390125 μg/ml） were designed to make cytotoxicity test. The largest concentration of dihydroartemisinin without cytotoxicity was chosen for the following tests. Hepatic stellate cells were cultured in vitro

which were divided into the normal control group

the iron deposition model group [25 μmol/L ferric ammonium citrate（FAC） ]

the deferoxamine group（50 μmol/L deferoxamine）

the dihydroartemisinin group（dihydroartemisinin）

the iron deposition +dihydroartemisinin group（25 μmol/L FAC + dihydroartemisinin） and the deferoxamine + dihydroartemisinin group（50 μmol/L deferoxamine + dihydroartemisinin）. All cells were cultured for 24 h. The expressions of cells’ αsmooth muscle actin（α-SMA） in all groups were detected with immunohistochemical method. The iron metabolism and the mRNA expressions of cell activation correlation factors [including hepcidin

transferrin receptor 1（TfR1）

and collagen I and Transforming Growth Factor β1（TGF-β1） ]were detected with polymerase chain reaction（PCR） method.Results Dihydroartemisinin with the concentration of 6. 25 μg/ml was chosen to be tested. There were a lot of cells’ α-SMA expressions in the iron deposition model group. Cells’ α-SMA expressions in the medicine groups were less than those in the normal control group and the iron deposition model group. Hepcidin mRNA expressions in the iron deposition model group decreased

while after being intervented with deferoxamine and/or dihydroartemisinin

hepcidin mRNA expressions increased（P < 0. 05）. The mRNA expressions of TfR 1

as well as collagen I and TGF-β1decreased in the dihydroartemisinin group

the FAC + dihydroartemisinin group and the deferoxamine + dihydroartemisinin group. Conclusion Dihydroartemisinin might have anti hepatic fibrosis effect in vitro. The mechanism might relate to regulating iron metabolism in cell and inhibiting hepatic stellate cell activation.