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目的 探讨米非司酮 (RU486 )在早孕滋养细胞信号传导及其凋亡中的影响。方法 2 19例服用RU486早孕药物流产者 ,对其有效组 30例 ,失败组 2 3例 ,人流组对照 16例 ,以免疫组化法分别标记孕激素受体(PR)、雌激素受体 (ER)、表皮生长因子受体 (EGFR)、酪氨酸蛋白激酶C(αPKC)、分裂激活蛋白激酶 (MEK - 1)、细胞转化分裂介质 (raf- 1)和抗凋亡蛋白 (Bcl- 2 )。三组均计数凋亡指数 (AI)。有效组与失败组各 5例观察透射电镜下凋亡改变。结果 有效组PKC、raf- 1、MEK - 1、Bcl- 2的表达有明显抑制 (P <0 0 5 ) ;AI为 0 19%。失败组信号传导受抑主要为PR、ER和EGFR(P <0 0 1) ,AI为 0 11%。结论 RU486抑制早孕滋养细胞PKC信号通路及raf- 1瀑布激酶链和分裂激活蛋白 ,抑制增生分裂分化并诱导凋亡发生 ;而失败组可能在PR、ER和EGFR信号传导初始阶段发生受体介质功能紊乱和抑制
Objective To investigate the effects of mifepristone (RU486) on signal transduction and apoptosis of gestational trophoblast cells. Twenty-two of the 19 abortion-taking abortion pregnant women with RU486 in the early pregnancy had 30 cases in the effective group, 23 cases in the failure group and 16 cases in the abortion group. The levels of progesterone receptor (PR), estrogen receptor ER, EGFR, αPKC, MEK - 1, raf - 1 and Bcl - 2 ). Three groups were counted for apoptosis index (AI). Five cases in the effective group and the failure group were observed apoptosis under the transmission electron microscope. Results The expressions of PKC, raf - 1, MEK - 1 and Bcl - 2 in the effective group were significantly inhibited (P <0.05); AI was 0 19%. The inhibition of signal transduction in the failure group was mainly PR, ER and EGFR (P <0.01), AI was 0 11%. Conclusions RU486 can inhibit the PKC signaling pathway and the raf-1 cascade and mitogen-activated protein in the first trimester of pregnancy, and inhibit the proliferation, differentiation and induction of apoptosis. In the failure group, the receptor mediators may occur during the initial stages of PR, ER and EGFR signaling Dysfunction and depression