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目的:研究孕激素对孕激素受体M(PR-M)阳性原代子宫肌瘤细胞生长的作用,并探讨其机制。方法:收集2015年9月到2016年6月在郑州大学第三附属医院妇科因子宫肌瘤行全子宫切除的肌瘤标本,原代培养细胞成功后用Western blot分别检测筛选出PR-M(+)/PR-A/B(-)的标本作为实验组和PR-M(-)/PR-A/B(+)作为对照组。用不同浓度米非司酮(MIF)处理,培养48h后,应用MTT法和流式细胞仪分别检测其对PR-M阳性和PR-M阴性子宫肌瘤细胞增殖和凋亡的影响。结果:随着浓度的增加与作用时间的延长,PR-M(+)和PR-M(-)子宫肌瘤细胞生长均受到抑制,浓度≥1×10~(-6)mol/L MIF处理48h后,两组肌瘤细胞的增殖抑制率和凋亡率逐渐增加,呈浓度和剂量依赖性(均<0.05)。其中PR-M(+)组肌瘤细胞各浓度增殖抑制率和凋亡率均小于PR-M(-)组,差异有统计学意义(均<0.05)。结论:MIF对PR-M原代培养子宫肌瘤细胞凋亡的作用和抑制增殖的作用时间-剂量依赖性。孕激素可能通过PR-M抑制原代培养子宫肌瘤细胞的凋亡促进肌瘤的发生发展,这种作用可被孕激素受体拮抗剂阻断。
Objective: To study the effect of progesterone on progesterone receptor M (PR-M) -positive primary uterine fibroids and its mechanism. Methods: From September 2015 to June 2016, a total of hysterectomy fibroids were collected from the Department of Gynecology, Third Affiliated Hospital of Zhengzhou University. Primary cultured cells were collected and screened for PR-M + / PR-A / B (-) as experimental group and PR-M (-) / PR-A / B (+) as control group. After being treated with different concentrations of mifepristone (MIF) for 48h, the effects of MIF on the proliferation and apoptosis of PR-M positive and PR-M negative uterine fibroids were detected by MTT assay and flow cytometry respectively. Results: The growth of uterine fibroids of PR-M (+) and PR-M (-) were inhibited with the increase of concentration and duration of action, and the concentration of MIF was ≥1 × 10 -6 mol / L After 48h, the proliferation inhibition rate and apoptosis rate of fibroids increased gradually in both concentration and dose dependent manner (all <0.05). The PR-M (+) fibroid cell proliferation inhibition rate and apoptosis rate were less than PR-M (-) group, the difference was statistically significant (all <0.05). Conclusion: The effect of MIF on the apoptosis of uterine fibroids in PR-M primary culture and the effect of inhibiting proliferation are time-dose dependent. Progesterone may promote the development of fibroids by inhibiting the apoptosis of primary cultured uterine fibroids by PR-M, and this effect may be blocked by progestin receptor antagonists.