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目的 探讨米非司酮对子宫肌瘤细胞凋亡和雌孕激素受体 (ER、PR)的影响以及凋亡与受体的关系。方法 12例子宫肌瘤患者 ,于月经周期第 15～ 16天口服米非司酮 2 5mg d ,连服 7d后行子宫切除术 ,取瘤体和子宫肌组织 ,行流式细胞术结合形态学变化检测瘤细胞凋亡 :做免疫组化观察ER、PR变化 ,9例分泌中期手术的肌瘤患者做对照组 ,同时取增生期 10例、分泌晚期 8例、月经期 5例以排除激素变化对瘤细胞凋亡及受体的影响。结果 服米非司酮后子宫肌瘤细胞凋亡指数、促凋亡基因bax含量明显升高 (P <0 .0 1) ,S期细胞比率 (SPF)、PR含量明显下降 (P <0 .0 1) ,抑凋亡基因bcl 2无明显变化 (P >0 .0 5 )。结论 首次证实米非司酮促进子宫肌瘤细胞凋亡 ,米非司酮通过降低瘤体内PR含量 ,增强bax基因表达的共同作用诱导瘤细胞凋亡 ,为其治疗子宫肌瘤的机制之一。
Objective To investigate the effect of mifepristone on the apoptosis of uterine fibroids and estrogen and progesterone receptor (ER, PR) and the relationship between apoptosis and receptor. Methods Twelve cases of uterine fibroids were treated with oral mifepristone 25 mg d on days 15-16 of the menstrual cycle. After 7 days of continuous hysterectomy, the tumors and uterine myometrium were removed. Flow cytometry and morphometry Changes in the detection of tumor cell apoptosis: immunohistochemical observation of ER, PR changes in 9 cases of secretory fibroids in patients with mid-term surgery to do the control group, while taking the proliferation of 10 cases, 8 cases of late secretion, menstrual period in 5 cases to rule out hormone changes Effects on tumor cell apoptosis and receptor. Results After treatment with mifepristone, the apoptotic index of uterine fibroids and the expression of bax gene were significantly increased (P <0.01). The percentage of S phase cells (SPF) and PR were significantly decreased (P <0. There was no significant difference in apoptosis-inhibiting gene bcl 2 (P> 0.05). Conclusions It is the first time that mifepristone promotes the apoptosis of uterine leiomyoma cells. Mifepristone can induce the apoptosis of tumor cells by decreasing the PR content in the tumor and enhancing the expression of bax gene, which is one of the mechanisms of mifepristone treatment.