摘要
目的通过突变诱发剂二乙基亚硝胺(diethylnitrosamine,DEN)联合肿瘤增强剂苯巴比妥(phenobarbital,PB)诱发PLCε基因敲除小鼠建立肝脏肿瘤动物模型。方法随机选取出生12日龄的雄性PLCε-/-小鼠和PLCε+/+小鼠各40只(分别为实验组I、实验组Ⅱ),先腹腔注射DEN,4周龄后开始加饮PB药水,持续喂养;同样随机选取出生12日龄的雄性PLCε-/-小鼠和PLCε+/+小鼠各40只(分别为对照组Ⅰ、对照组Ⅱ)正常喂养;实验周期均为24周,实验结束后在电子显微镜下观察小鼠肝脏肿瘤的形成。结果经病理学结果证实,实验组Ⅱ小鼠发生肝脏肿瘤18只,成癌率为60%,实验组Ⅰ小鼠发生肝脏肿瘤15只,成癌率为46.9%。而对照组Ⅰ、Ⅱ的小鼠均未发生肝癌。结论利用突变剂DEN联合PB诱发PLCε基因敲除小鼠成功地建立了肝脏肿瘤模型,为进一步研究PLCε在肝脏肿瘤形成过程中的作用奠定了基础。
Objective To establish animal models of liver tumors, the PLCe gene knockout mice was induced by mutation inducers Diethylnitrosamine （ diethylnitrosamine DEN ） combined with tumor enhancer phenobarbital （phenobarbital PB）. Methods 12-day-old male PLCε -/ - and PLCε-/- mice were randomly selected as group I （n = 40）and group II （n =40）,respectively. The mice of group I and II were injected DEN through abdominal cavity at the age of 12 days, then drinking PB after 4 weeks and continuously until 24 weeks. At the same time, 12-day-old male PLCε -/ - and PLCε ＋ / ＋ mice were randomly selected as the control group I （n = 40） and control group H （n = 40） , respectively, and fed with normal feeds for 24 weeks. At the end of the experiment, the liver tumor was observed under electron microscopy. Results Pathology results confirm that 18 mice of group II had liver tumors, and rate of tumor formation is 60% ; 15 mice of group I had liver tumors, and rate of tumor formation is 46. 9% ; the mice of control group I and H had not liver tumors. Conclusions The animal model of liver tumor have been successfully established by using mutation inducers DEN combined with PB in PLCe gene knockout mice, and could provide a foundation for further researching effects of PLCε during liver tumor formation.
出处
《中国比较医学杂志》
CAS
2013年第3期17-20,I0002,共5页
Chinese Journal of Comparative Medicine
基金
北京市自然基金面上项目(7102144)
