Abstract: Objective To investigate the effects of iron deposition on the liver fibrosis and its potential mechanisms in rats. Methods 39 SD rats were randomly divided into fibrosis group（n=27） and control group （n=12）. Rats with hepatic fibrosis（n=27） were established by intraperitoneal injection of dimethylnitrosamine （DMN,10 μL.kg^-1）. After one-week DMN injection,the 27 rats were randomly divided into model group （n=15） and desferrioxamine group（n=12）. At the beginning of the third week,rats in model and desferrioxamine group were respectively injected intraperitoneally with normal saline or desferrioxamine at the dose of 100 mg·kg^-1·d^-1,3 times per week for 2 weeks before they were sacrificed. Liver tissues were stained with HE,Masson and Prussian blue,respectively;Immunohistochemistry was applied for the detection of α-smooth muscle actin （α-SMA） expression;Hepatic iron concentration （HIC） in liver tissues were evaluated by flame atomic absorption spectrophotometry（FAAS）;ELISA was adopted to examine the concentrations of serum ferritin and transferrin. Automatic biochemical analyzer was used to detect the liver function and the serum level of iron. The mRNA levels of transforming growth factor-β1（TGF-β1） was detected by quantitative PCR. Results Our histopathological findings showed that iron loads in liver tissues in model group increased obviously,accompanied with excessive collagen deposition,hepatocyte denaturation and necrosis and activation of a great number of hepatic stellate cells （HSCs） and the iron distributed in fibrous septa with main deposition in Kupffer cells（KCs） and HSCs;The hepatic iron concentration in model group [（0.778±0.098） mg/g] was higher than that in control group[（0.436±0.043） mg/g,LSD-t=5.15,P<0.01] and than in desferrioxamine group[（0.595±0.146） mg/g,LSD-t=-2.76,P<0.05];Compared with in control,the level of serum ferritin in model group significantly increased,and the level of serum transferrin obviously decreased [ferritin,（47.657±27.851） ng/mL vs.（24.166±27.626） ng/mL,LSD-t=2.21,P<0.05;transferrin,（0.322±0.099） mg/mL vs.（0.653±0.170） mg/mL,LSD-t=-4.78,P<0.01];Compared with in the model group,the serum level of ferritin had reduced and the serum level of transferrin increased in desferrioxamine group [ferritin,（10.261±12.466） ng/mL vs. （47.657±27.851） ng/mL,LSD-t=-3.52,P<0.01;transferrin,（0.584±0.180） mg/mL vs.（0.322±0.099） mg/mL,LSD-t=3.77,P=0.01];Compared with in control,TGF-β1 mRNA in model group was significantly up-regulated [（11.896±0.639） vs. （2.292±0.222）,LSD-t=25.95,P<0.01],which decreased as compared with in desferrioxamine group[（7.481±0.745）,LSD-t=-11.95,P<0.01]. Conclusion Iron deposition in the liver may play an important role in the onset and development of hepatic fibrosis. The potential mechanism might be related to iron deposition in KCs and HSCs,facilitating the activation of HSCs.

Key words: Liver fibrosis, Iron, Desferrioxamine, Hepatic stellate cell, Kupffer cell, Rats