中文摘要：

目的：探讨血清GP73、AFP在DEN／CCl4／乙醇联合诱发的小鼠肝癌模型中的表达及意义。方法：60只BALB／C小鼠随机分为实验组（50只）和正常对照组（10只），联合DEN／CCl4／乙醇诱发小鼠肝癌模型，于第4、8、12、16、20、24周随机分批处死实验小鼠，采血及常规制作肝脏病理切片，采用酶联免疫吸附测定（ELISA）方法检测小鼠肝脏癌变过程中不同时期血清GP73、AFP的表达情况。结果：诱癌组小鼠第4-8周肝脏呈现出典型的药物中毒性肝炎表现，血清GP73、AFP仅见微弱表达，与正常对照组无统计学上的差异（P〉0．05）。第12-16周血清GP73、AFP随肝纤维化不断加重呈逐渐升高趋势，至第20周后肝癌形成时（诱癌第20-24周），GP73、AFP升高最为显著，结果具有统计学意义（P〈0．05）；且GP73及AFP之间呈正相关关系（r=0．79，P=0．00）。结论：GP73、AFP参与小鼠肝癌的发生发展，其机制可能与二者在肝细胞大量损伤、增生过程中被激活，随肝癌形成相互作用有关。

英文摘要：

Objective：To explore the expression and biological significance of both GP73 and AFP during experi- mental hepatoearcinogenesis in mouse. Methods：Fifty BALB/C mice were induced to establish primary hepatocellular carcinoma （HCC） models by combination of diethylnitrosamines （DEN）, carbon tetrachloride （CC14 ） and ethanol for twenty -four weeks, then the occurrence and development of HCC were observed, and other ten BALB/C mice were used as normal control （ no drug was given）. The serum levels of GP73 and AFP were detected by enzyme linked im- munosorbent assay （ELISA）. Results：In the case group, toxic hepatitis and acute hepatocellular necrosis were ob- served in carcinogenesis mouse in 4 -8weeks, serum GP73 and AFP only saw a slight expression, there was no statis- tically significant difference with normal control group（ P 〉 0.05 ）. In 12 - 16weeks, serum GP73 and AFP with liver fibrosis increasing trend was gradually increased, to the formation of hepatocellular carcinoma after 20 -24weeks, GP73 and AFP elevated to the most significant results had statistically significant （ P 〈 0.05 ）. And a positive correla- tion between GP73 and AFP （ r = 0.79, P = 0.00 ） was seen. Conclusion ： An BALB/C mouse liver cancer model was established by induction with combination of DEN, CC14 and ethanolin a relatively short time. Serum level of GP73 and AFP in the carcinogenesis and progression of HCC can be used as a suitable marker for early detection of the cancer- ous process