Abstract: Objective To investigate the dynamic change of hepcidin in liver fibrosis induced by CCl4 among mice. Methods C57 BL /6mice were given CCl4 by intragastric administration to establish a liver fibrosis model. The degree of liver injury and fibrosis was evaluated by HE and Masson staining. Prussian blue staining was used to detect liver iron deposition in the progression of liver fibrosis. Primary hepatocytes,hepatic stellate cells,and Kupffer cells were isolated from C57 BL /6 mice by two- step in situ collagenase perfusion and density gradient centrifugation. The mRNA levels of tumor necrosis factor alpha( TNFα),interleukin- 6( IL- 6),interleukin- 1β( IL- 1β),and hepcidin were measured by quantitative real- time PCR( qRT- PCR). Continuous data were expressed as mean ± SD,and comparison of continuous data between the two groups was made by t test. Results The HE and Masson staining of liver tissues showed that the degree of liver fibrosis gradually increased as CCl4 was given,and hepatic fibrosis was reversed after the administration of CCl4 was stopped. Prussian blue staining showed that liver iron deposition increased as CCl4 was given; the area of liver iron deposition was significantly increased compared with that of the normal control group at week 4 of administration( t = 4. 772,P < 0. 05),but no significant increase was seen from week 4 to week 6; the area of liver iron deposition at week 6 was still higher than that of the normal control group( t = 10. 32,P < 0. 05);liver iron deposition decreased in the spontaneous reversal after the administration was stopped. The mRNA levels of TNFα,IL- 1β,and IL-6 assessed by qRT- PCR continuously increased in model mice,reaching the peak levels at week 6,and significant differences were observed between the model mice and normal controls( t = 4. 322,9. 707,and 5. 678,P < 0. 05 for all). The expression of hepcidin in the liver increased in the early stage of model establishment and reached the peak level at week 4,with a significant difference compared with that of the normal control group( t = 2. 590,P < 0. 05),but it was reduced in the spontaneous reversal. Conclusion Liver iron deposition increases gradually in the progression of liver fibrosis induced by CCl4 among mice. The expression of hepcidin in the liver is upregulated in the progression of liver fibrosis and is correlated with the expression of inflammatory cytokines.