抑癌基因PTEN在孕三烯酮诱导子宫内膜异位症细胞凋亡中的作用

目的　研究抑癌基因PTEN在孕三烯酮诱导体外培养的子宫内膜异位症细胞凋亡中的作用。方法　以不同浓度的孕三烯酮对体外培养人子宫内膜异位症细胞进行处理 ,MTT法测算孕三烯酮作用 0～ 4 8h对子宫内膜异位症细胞的抑制情况并绘制生长曲线 ;取 2 4h为作用时间 ,透射电镜观察细胞超微结构变化 ,流式细胞仪检测细胞凋亡率及细胞周期 ,应用PTEN单克隆抗体经由流式细胞仪分析细胞内PTEN的表达。结果　细胞生长曲线显示孕三烯酮对子宫内膜异位症细胞的生长增殖有显著的抑制作用 ,且呈时间 剂量 效应关系 ;透射电镜观察发现 ,孕三烯酮可诱导子宫内膜异位症细胞发生典型的凋亡形态学改变 ;流式细胞仪检测显示 1× 1 0 -6mol/L和1× 1 0 -4mol/L浓度的孕三烯酮作用 2 4h后 ,子宫内膜异位症细胞的凋亡率分别为 1 3%和 1 5 0 % ,与对照组相比差异显著 ;同时细胞内PTEN的表达有不同程度的上调。结论　孕三烯酮能明显抑制子宫内膜异位症细胞的生长增殖 ,这一作用可能与上调PTEN的表达及诱导细胞凋亡有关

Role of tumor suppressor gene PTEN in apoptosis of isolated ectopic endometrial cells induced by gestrinone

Objective To investigate the role of tumor suppressor gene PTEN(phosphatase and tension homologue deleted on chromosome 10,PTEN)in apoptosis of ectopic endometrial cells induced by gestrinone. Methods Ectopic endometrium cells obtained from endometriosis were cultured and exposed to gestrinone in different concentrations. The inhibition of the cells during 48 hours was determined by MTT assay, and the cell growth curve was plotted. Then the morphological changes in cells treated with gestrinone for 24h were observed with transmission electron microscope, and the apoptosis rate, cell cycle of the cells and PTEN expression were assessed with flow cytometry analysis (FCM) at the same time. Results Gestrinone in different concentrations could inhibit the growth and proliferation of ectopic endometrium cells in a does and time dependent manner, and the cell growth curve was changed accordingly. After 24 hours exposure to gestrinone in the concentrations of 10 -6 to10 -4 mol/L, some apoptotic changes were observed in the cells under transmission electron microscope. FCM showed that after the exposure to gestrinone, the apoptotic rate of ectopic endometrial cells was 1.3% in 10 6 mol/L group and 15.0% in 10 -4 mol/L group, indicating that there was significantly increase in apoptosis when compared with the control group. At the same time the level of PTEN expression was also increased. Conclusion Gestrinone can significantly inhibit the growth and proliferation of ectopic endometrial cells in endometriosis, and this effects seems to be related to an increase in PTEN expression.