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目的:探讨信号转导和转录激活因子3(STAT3)在小鼠胚泡植入过程中的生物学作用。方法:将孕鼠随机分为米非司酮组、溶剂组和空白对照组,用免疫组织化学技术和图像分析方法检测各组小鼠孕3～8 d子宫内膜中STAT3的动态表达,并对其进行半定量分析。结果:溶剂组和对照组小鼠子宫内膜中STAT3的表达在孕3 d明显增强,孕4 d达到峰值,且溶剂组和对照组间在孕3～8 d各时间点的表达差异无统计学意义;米非司酮组STAT3的表达较2个对照组显著降低(P<0.01),在孕4 d亦无表达高峰。结论:STAT3是介导胚泡植入的重要因子之一,米非司酮可能通过抑制孕激素与其受体结合而下调STAT3的表达,影响子宫内膜容受性的建立,阻碍胚泡顺利植入。
Objective: To investigate the biological role of signal transducer and activator of transcription 3 (STAT3) in the mouse blastocyst implantation. Methods: Pregnant mice were randomly divided into mifepristone group, solvent group and blank control group. Immunohistochemistry and image analysis were used to detect the dynamic expression of STAT3 in the endometrium from 3 to 8 d of pregnancy The semi-quantitative analysis. Results: The expression of STAT3 in the endometrium of the solvent group and the control group increased significantly on the 3rd day of pregnancy and peaked on the 4th day of pregnancy, and there was no statistical difference in the expression of STAT3 between the solvent group and the control group at 3 ~ 8 d of pregnancy Significance of STAT3 expression in the mifepristone group was significantly lower than that in the two control groups (P <0.01), and no peak at 4 d after pregnancy. CONCLUSIONS: STAT3 is one of the important mediators of blastocyst implantation. Mifepristone may down-regulate the expression of STAT3 by inhibiting the binding of progesterone to its receptor, thus affecting the establishment of endometrial receptivity and inhibiting the smooth blastocyst Into.