摘要目的研究米非司酮配伍米索前列醇药物流产后蜕膜纤溶酶原激活剂及其抑制物（PA、PAI）变化，探讨药物流产后异常子宫出血的机理。方法 45例早孕受试者随机平均分成3组：正常蜕膜组、米非司酮组和米非司酮米索前列醇药物流产组。应用逆转录－聚合酶链反应（RT-PCR）技术、发色底物法和酶联免疫吸附试验（ELISA）法观察3组蜕膜组织型纤溶酶原激活剂（tPA）和I型纤溶酶原激活剂抑制物（PAI-1）mRNA及蛋白表达水平。结果米非司酮米索组和米非司酮组tPA活性分别为46.91±20.74IU/mg protein和64.25±35.81IU/mg protein，低于正常蜕膜组（P<0.05）； tPA mRNA水平以米非司酮米索组最高（1.43±0.39，P<0.05），而另2组之间无差异（P>0.05）；PAI-1 mRNA和蛋白水平3组间均无差异（P>0.05）。结论米非司酮和米索前列醇经转录后途径降低人早孕子宫蜕膜tPA活性，可影响蜕膜剥落、血管再生、内膜复修而致药物流产后子宫出血时间过长。

abstractsObjective　To investigate the mechanism of prolonged uterine hemorrhage after terminating early pregnancy by mifepristone plus misoprostol.Methods　Forty-five decidua specimens were obtained from 45 pregnant women with amenorrhea of 6-7 week duration. Fifteen women were treated with mifepristone and 15 were treated with mifepristone plus misoprostol. The remaining 15 served as controls. The tPA and PAI-1 mRNA levels were estimated by reverse transcription-polymerase chain reaction. Chromogenic assay and enzyme-linked immunosorbent assay were used to detect tPA activity and PAI-1 protein level in decidua. Results　The activities of tPA in the mifepristone plus misoprostol group and in the mifepristone group were 46.91±20.74?IU/mg*protein and 64.25±35.81?IU/mg*protein respectively, lower than those in the normal decidua group (99.76±58.61?IU/mg*protein, P<0.05). tPA mRNA levels in the mifepristone plus misoprostol group were the highest (1.43±0.39) among the groups. In the mifepristone group, tPA mRNA level (0.90±0.16) was not significantly different from that in the normal decidua group (0.94±0.17). The protein and mRNA expression levels of PAI-1 were not significantly different among the three groups (P>0.05).Conclusions　Mifepristone plus misoprostol decreased tPA activity in human early decidua by post-transcription pathways, which may influence decidua shedding, endometrial angiogenesis, endometrial remodeling, and cause prolonged uterine hemorrhage after drug abortion.