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降低血清IGF-1水平抑制乳腺肿瘤细胞增殖的实验研究 被引量:1

The experimental study of low serum IGF-1 level inhibit mammary tumor cell proliferation
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摘要 目的在肝特异性胰岛素样生长因子1(IGF-1)基因缺失小鼠及对照鼠体内建立原发性乳腺癌,探讨血清中IGF-1水平与乳腺肿瘤细胞增殖的关系。方法使用7,12-二甲基苯蒽(DMBA)在实验鼠体内诱导原发性乳腺癌,人参皂甙Rg3进行干预治疗。比较各组肿瘤发生情况,流式细胞术检测细胞周期及凋亡比例。结果未管饲Rg3的对照鼠乳腺癌发病率为66.67%,显著高于其他各组(P〈0.05);而管饲Rg3的肝特异性IGF-1基因缺失(LID)鼠乳腺癌发病率为12.00%,显著低于其他各组(P〈0.05)。未管饲Rg3的对照鼠凋亡比例为(2.47±0.69)%,低于其他各组(P〈0.05);而管饲Rg3的LID鼠凋亡比例为(14.00±1.74)%,高于其他各组(P〈0.05)。结论降低血清IGF-1水平可促进细胞凋亡,对乳腺肿瘤的发生具有抑制作用,人参皂甙Rg3对这一效应具有协同作用。 Objective A stable primary mammary tumor model in liver-specific insulin-like growth factor Ⅰ (IGF-1) deficient (LID) mice and control mice was established. The potential relationship between circulating IGF-1 level and proliferation of mammary tumor was explored. Methods Induction of mammary tumors was achieved by using 7,12-dimethybenz (a) anthracene (DMBA) in experimental mice. Ginsenoside Rg3 was used in treatment. The incidence of mammary tumor in every group was compared, and the cell cycle and apoptosis percentage were determined by flow cytometry. Results The incidence of tumor in untreated control mice was 66. 67%, which was significantly higher than that in any other group ( P 〈0. 05). The incidence of tumor in Rg3-treated LID mice was 12. 00% , which was significantly lower than that in any other group ( P 〈0. 05). The apoptosis percentage in untreated control mice was (2. 74±0. 69)% , which was significantly lower than that in other groups ( P 〈 0. 05 ). The apoptosis percentage in Rg3-treated LID mice was ( 14. 00 ± 1.74) % , which was significantly higher than that in other groups ( P 〈 0. 05 ). Conclusion Low serum IGF-1 level is able to promote tumor cell apoptosis, which consequently inhibit the growth of breast cancer. There is a synergistic effect with the application of ginsenoside Rg3.
出处 《中国医师杂志》 CAS 2007年第12期1607-1609,共3页 Journal of Chinese Physician
基金 国家自然科学基金资助项目(30271280),湖北省自然科学基金资助项目(2002AB129)
关键词 胰岛素样生长因子Ⅰ 乳腺肿瘤 细胞增殖 Insulin-like growth factor Ⅰ Breast neoplasms Cell proliferation
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参考文献8

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