中文摘要：

目的证实肝硬化组织中存在人肝脏祖细胞（HPCs），探讨HPCs分布及激活的强度与肝脏炎症程度的关系，提供HPCs向肝细胞分化的依据。方法对30例肝硬化及3份正常组织标本进行常规组织学观察，对门静脉炎症程度进行评分，并用胆管上皮标志物（细胞角蛋白7）和肝星状细胞激活标志物（a平滑肌肌动蛋白）进行免疫组织化学染色，对符合HPCs、中间型肝细胞以及小管样反应的细胞进行计数和半定量评分。结果在正常肝组织中无门静脉周围HPCs和小管样反应增殖。在肝硬化组织中，增殖的HPCs起源于肝门静脉区域，随着门静脉炎症程度加重，HPCs及小管样反应从肝硬化结节周围向肝实质扩散并出现中间型肝细胞增殖，其周围有显著的肝星状细胞激活。HPCs及小管样反应增殖程度随着门静脉炎症程度的加重而增加。HPCs数目与中间型肝细胞数目之间存在直线正相关。丙氨酸氨基转移酶和天冬氨酸氨基转移酶与HPCs及中间型肝细胞数目存在直线正相关。结论在人肝硬化中存在祖细胞的激活，炎症反应是HPCs激活的触发因素，HPCs向肝实质内迁移并向肝细胞方向分化是肝再生的重要途径。

英文摘要：

Objective To confirm whether human hepatic progenitor cells （HPCs） occur in human liver cirrhosis, to investigate the relationship between the degree of HPCs activation and the degree of liver inflammation and to provide evidence that HPCs can differentiate into hepatocytes. Method Surgical specimens from 30 human cirrhostic livers and from 3 normal livers were investigated by light microscopy and immunohistochemical staining for CK7 （a marker of biliary differentiation） and SMA （a marker of hepatic stellate cell activation）. The degree of portal inflammation was determined on routine stained sections. The number of HPCs and intermediate hepatocytes and the extent of the ductular reaction were assessed. Results HPCs and ductular reaction were not observed in the normal livers. In liver cirrhosis cases the HPCs originated from the portal areas. With the increase of portal inflammation, HPCs and ductular reaction extending from the periphery of the liver cirrhosis nodules to the liver parenchyma and the intermediate hepatocyte proliferation were observed. The notable hepatic stellate cell activation occured around the HPCs and ductular reaction. The number of HPCs and the extent of ductular reaction increased significantly as the portal inflammation increased. There were significant correlations between the number of HPCs with the number of intermediate bepatocytes. In addition, there was a strong correlation between the ALT and AST with the number of HPCs and intermediate hepatocytes. Conclusion Human hepatic progenitor cell activation exists in human liver cirrhosis. The inflammation is a trigger for HPCs activation. HPCs migration from the portal area to liver parenchyma and their differentiation into hepatocytes are important pathways for liver regeneration.