目的 通过对RSA患者和正常早孕女性绒毛、蜕膜中Survivin、VEGF及Stat3的测定,探讨不明原因反复流产患者的病因和母-胎界面滋养细胞增殖的调控机制.方法 采用免疫组化法检测40例反复自然流产(RSA)患者及20例对照组的绒毛和蜕膜组织中Survivin、VEGF及Stat3含量.结果 RSA患者绒毛组织中Survivin、VEGF的表达水平高于正常妊娠组,差异有统计学意义(P<0.05),二者在绒毛中的表达呈正相关(r=0.268,P<0.05);RSA组与正常对照组的绒毛中Stat3的表达差异无统计学意义(P>0.05),Survivin与Stat3的表达不存在相关关系(r=-0.006,P>0.05);RSA组与正常对照组蜕膜中Survivin、VEGF和STAT3的表达差异无统计学意义(P>0.05).结论 本研究发现在胚胎发育和胎盘形成过程中VEGF通过上调Survivin,促进细胞增殖、血管形成和抗细胞凋亡的作用,参与胚胎着床、胎盘生长和浸润;而Stat3与其无关,RSA胚胎凋亡时Survivin的上调可能不通过JAK-STAT途径.%Objective To investigate the pathogenesis of recurrent spontaneous abortion ( RSA ) and the regulation mechanism of trophoblast cell proliferation on matenal-fetal interface through measuring the levels of Survivin,VEGF and Stat3 in villus and decidua in women with RSA. Methods The levels of Survivin, VEGF and Stat3 in villus and decidua in 40 women with RSA ( observation group ) and 20 healthy subjects ( control group ) were detected. Results The expression levels of Survivin and VEGF in villus in women with RSA were significantly higher than those in normal pregnant women during the first trimester ( P < 0. 05 ), and the expression levels of Survivin in observation group were positively correlated with those in control group ( r = 0. 268, P < 0.05 ). However there was no significant difference in the expression levels of Stat3 in villus between the two groups during the first trimester ( P > 0. 05 ). There was no correlation in the expression levels in villus between VEGF and Survivin ( r = -0. 006, P >0. 05 ), furthermore, there were no significant differences in the expression levels of Survivin, VEGF and Stat3 in decidua between the two groups ( P >0. 05 ). Conclusion The results in the investigation suggest that VEGF can promote cell proliferation, angiopoiesis and antiapoptotic effect during embryo development and placentation by up-regulating the expression of Survivin, which is involved in embryo nidation, placenta development and infiltration, however, Stat3 is not related with VEGF, furthermore, the up-regulation of Survivin expression during embryo apoptosis may not carry out via signal transducer and activator of transcription-3 pathway.
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