中文摘要：

目的观察生理性雌激素在化学性诱导大鼠肝癌生成过程中的作用。方法将5周龄雌性SD大鼠192只分成4组：诱癌对照组（n=46）、假手术组（n=47）、去卵巢组（n=50）、去卵巢＋雌激素组（n=49）。联合应用二乙基亚硝胺（DEN）和N-亚硝基吗啉（NMOR）建立诱导性大鼠高转移肝癌模型，去卵巢＋雌激素组大鼠使用生理剂量雌激素进行干预。诱癌20周后，分析各组大鼠肿瘤生成、发展、转移和生存情况。结果诱癌20周后，去卵巢＋雌激素组大鼠肝癌生成率（44．44％）、肺转移率（20．00％）和肝肿瘤平均直径（0．39±0．24）cm均低于去卵巢组（分别为92．59％、65．21％和（0．95±1．22）cm，差异有统计学意义（P〈0．05）；实验终点前去卵巢＋雌激素组死亡大鼠生存时间（79．54±4．14）d也显著长于去卵巢组（59．54±8．31）d（P〈0．05）。结论生理性雌激素抑制大鼠肝癌的生成、发展和转移。

英文摘要：

Objective To examined the effect of estrogen, at physiological concentrations, on our established hepatocellular carcinoma （HCC） rat model induced by diethylnitrosamine and N-nitrosomorpholine. Methods Female Sprague-Dawley rats were randomly divided into four groups （group 1, control; group 2, shank-operated; group 3, ovariectomy; group 4, ovariectomy ＋estrogen） with treatment of a single i.p. injection of diethylnitrosamine （ 100 mg/kg body weight） and following N-nitrosomorpholine （ 100 ppm） in drinking water for 20 weeks for establishment of the rat HCC model. Physiological estrogen was administered by 17α-ethynylestradiol at a dose of 30 μg/kg body weight, and those in group 2 were treated with saline after initiation of liver carcinogenesis. Results The incidence of HCC （44. 44% ） , the lung metastasis rate （20. 00% ） and the mean liver nodules （0. 39 ±0. 24） cm were reduced in group 4 than in group 3 [92.59%, 65.21%, （0. 95 ±1.22） cm respectively] （P 〈0. 05） ; The survival time in group 3 was significantly shorter than in group 4 （ P 〈 0. 05 ）. Conclusion Estrogen, at physiological concentrations, may reveal a protective role in hepatocareinogenesis.