中文摘要：

目的利用四氯化碳（CCl4）肝纤维化小鼠模型,动态观察小鼠肝纤维化发生发展过程中血清铁、肝脏组织铁的变化及血清铁调素（hepcidin）对铁代谢的影响,为临床抗肝纤维化治疗提供实验依据。方法利用8周龄的C57BL/6品系雄性小鼠分别给予CCl4一周2次灌胃建立不同时期的肝纤维化模型,通过HE及Masson染色观察各组小鼠肝脏炎症、肝损伤及纤维化程度,并通过检测小鼠血清铁调素、血清铁、肝脏组织铁、膜铁转运蛋白的表达来评价小鼠肝纤维化过程中铁调素对铁代谢的影响。结果 CCl4肝纤维化模型小鼠随造模时间的延长,纤维化程度逐渐加重,血清铁调素的表达呈递增趋势;血清铁及肝脏组织铁均呈先增加后降低的趋势,但两者出现峰值的时间点不同,且在CCl4灌胃第6周仍高于正常对照组。血清膜铁转运蛋白随时间变化趋势与肝脏组织铁相似。结论在CCl4诱导的肝纤维化小鼠模型中,随纤维化程度逐渐加重,血清铁调素的表达逐渐增加;血清铁、肝脏组织铁及膜铁转运蛋白的表达呈先增加后降低趋势,与铁调素调控体内铁代谢、维持铁稳态密切相关,同时也证实了肝纤维化过程中存在铁沉积。

英文摘要：

Objective To explore the dynamic changes of serum iron,iron in hepatic tissue and the effect of serum hepcidin on iron metabolism during the development of liver fibrosis in mouse model. Methods Wild type C57 BL /6 mice（ 8 weeks old males） were given with carbon tetrachloride（ CCl4） to induce liver fibrosis. Liver injury and fibrosis were evaluated by HE and Masson staining. The iron metabolism during the process of liver fibrosis in mice were evaluated by detecting the expression of serum hepcidin,serum iron,iron in hepatic tissue and serum ferroportin. Results Following the degree of liver fibrosis gradually increased,the expression of serum hepcidin was upregulated. Serum iron,iron in hepatic tissue and serum ferroportin were increased at the beginning and then decreased,while the peak time was different. There was a positive correlation between serum ferroportin and iron in hepatic tissue. Conclusion In mouse model of liver fibrosis induced by CCl4,the expression of serum hepcidin is continuously increased. Serum iron,iron in hepatic tissue and serum ferroportin are increased at the beginning and then decreased. Hepcidin has a regulatory role in the expression of serum iron and iron in hepatic tissue of mice. It has also been confirmed that deposition of iron is present in the process of hepatic fibrosis.