生理性雌激素对大鼠肝癌生成的保护作用

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.

Abstract：

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, sham-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 hepatocarcinogenesis.

Protective effects of physiological doses of estrogen during hepatocarcinogenesis in a rat model

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, sham-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 hepatocarcinogenesis.