C57BL/6J小鼠肝癌动物模型的建立  

Establishment of C57BL/6J mouse liver cancer model

作　　者：匡志鹏[1] 谢裕安[1] 杨帆[1] 梁安民[1] 罗小玲[1] 吴继宁[1] 

机构地区：[1]广西肿瘤防治研究所生物医学研究中心,广西南宁530021

出　　处：《中国普通外科杂志》2007年第7期657-660,共4页China Journal of General Surgery

基　　金：国家自然科学基金资助项目(30360114)

摘　　要：目的建立C57BL/6J小鼠肝癌动物模型,为深入开展肝细胞癌的实验研究打下基础。方法取90只C57BL/6J小鼠,联合采用二甲基亚硝胺(DEN)/四氯化碳(CCl4)/乙醇诱导20周,观察其肝癌的发生情况。另取10只同种小鼠作为正常对照组。RT-PCR法检测病变肝组织中AFP基因表达。结果实验组90只小鼠共死亡8只;病理学检查发现,存活的82只小鼠中有71只发生肝癌,诱癌成功率为78.9%(71/90),肝癌小鼠的肝癌组织学类型以中、高分化为主;另11只有不同程度的药物中毒性肝炎或肝硬化(12.2%);对照组小鼠肝脏均未发现明显异常。成癌组中的肝癌组织RT-PCR检测可见AFP基因表达,非肝癌组织及对照组于组织中无AFP表达。结论采用DEN/CCl4/乙醇联合能诱导出C57BL/6J甲胎蛋白分泌型小鼠肝癌,诱导时间相对较短,癌变率高,部分病变肝组织中伴有肝炎、肝硬化病理学改变,是较理想的研究肝癌的实验动物模型。Objective To establish a stable primary hepatocellular carcinoma （HCC） model of C57BL/6J mice, and establish a basis for in-depth laboratory research in hepatocellular cancer. Methods Ninety C57BL/6J mice were induced to establish HCC models by combination of diethylnitrosamines （DEN）, carbon tetrachloride （ CCl4 ） and ethanol for twenty weeks, then the occurrence and development of HCC were observed, and other 10 C57 BL/6J mice were used as normal control（ no drug was given）. RT-PCR method was used to observe AFP mRNA expression in liver tissues and tumor tissues. Results seventy-one of 90 mice developed HCC（78.9 % ） , cirrhosis was observed in 11 of 90 mice（ 12.2 % ） , and 8 of them died of toxic hepatitis and acute hepatocellular necrosis. AFP mRNA was expressed only in liver cancer tissues. No obvious liver pathologic changes were observed in the control group. The histo-pathologic changes of HCC were high or middle differentiation. Conclusions An AFP-secreting C57BL/6J mouse liver cancer model was established by induction with combination of DEN, CCl4 and ethanol in a relatively short time. The rate of cancerous change was high, and some of the hepatic changes included hepatitis and cirrhosis. This is a rather ideal animal model for the study of liver cancer.

关 键 词：肝肿瘤 实验性 疾病模型 动物 小鼠 

分 类 号：R587.102[医药卫生—内分泌]