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目的:探讨米非司酮对人子宫内膜细胞凋亡和坏死的影响。方法:体外培养人子宫内膜细胞,采用不同浓度米非司酮处理,观察米非司酮对细胞形态的影响,MTT法检测米非司酮对细胞增殖能力的影响,检测米非司酮处理细胞后子宫内膜发育相关基因ESR1和PGR的含量、坏死途径蛋白p-MLKL、RIPK3的表达和凋亡途径蛋白Bax、procaspase3/caspase3的变化。结果:经米非司酮处理后,人子宫内膜细胞细胞形态明显变差,细胞增殖能力明显变弱,且随着米非司酮处理浓度增加,其对细胞生长的毒性作用加强;米非司酮处理的细胞中ESR1和PGR含量明显减少,而坏死途径蛋白p-MLKL、RIPK3表达和凋亡途径蛋白Bax、pro-caspase3/caspase3表达增加。结论:米非司酮可促进人子宫内膜细胞的凋亡和坏死而抑制其细胞增殖,其作用可能与调节ESR1/PGR含量、坏死途径蛋白p-MLKL/RIPK3及凋亡途径蛋白Bax/pro-caspase 3/caspase 3表达有关。
Objective: To investigate the effect of mifepristone on apoptosis and necrosis of human endometrium. Methods: Human endometrial cells were cultured in vitro and treated with mifepristone at different concentrations to observe the effects of mifepristone on cell morphology. The effect of mifepristone on the proliferation of cells was detected by MTT assay. The effect of mifepristone treatment The expression of ESR1 and PGR, the expression of p-MLKL, RIPK3 and the apoptosis pathway proteins Bax, procaspase3 / caspase3 in endometrial cells. Results: After mifepristone treatment, the cell morphology of human endometrial cells was obviously deteriorated and the cell proliferation ability was obviously weakened. With the increase of the concentration of mifepristone, the toxic effect on cell growth was strengthened. The levels of ESR1 and PGR were significantly decreased in the cells treated with progesterone, while the expressions of p-MLKL, RIPK3 and Bax and pro-caspase3 / caspase3 were increased. Conclusion: Mifepristone can promote apoptosis and necrosis of human endometrial cells and inhibit its proliferation, which may be related to the regulation of ESR1 / PGR content, p-MLKL / RIPK3 and Bax / pro -caspase 3 / caspase 3 expression.