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目的:探讨活化的β-连环蛋白(active β-catenin)在胚胎着床过程中的作用。方法:将孕第2日(d2)昆明小鼠随机分成3组,每组30只,A组:孕d2单次背部皮下注射0.1ml米非司酮(1.2mg/ml);B组(溶剂对照):以等量1,3-丙二醇代替米非司酮;C组:不作任何处理。用免疫组织化学、间接免疫荧光、Western blotting方法定性、定量、定位检测3组小鼠在妊娠d3￣7活化的β-连环蛋白的动态表达。结果:B、C组小鼠子宫内膜中活化的β-连环蛋白于孕d3在腺上皮和腔上皮、基质细胞质和细胞膜表达;妊娠d4在腔上皮细胞质和细胞膜强表达,并达高峰;妊娠d5￣7在腺上皮、血管内皮、腔上皮下基质细胞膜和细胞质表达,且B、C组间在妊娠d3￣7各时间点的表达无显著性差异(P>0.05);A组小鼠妊娠d3￣7活化的β-连环蛋白的表达较B、C组显著降低(P<0.01),在妊娠d4表达量未见高峰,且表达部位局限于基质细胞,腔上皮无表达。结论:米非司酮可能通过抑制孕激素与其受体结合而下调活化的β-连环蛋白表达,进而抑制子宫内膜黏附性,影响子宫内膜容受性的建立而阻碍胚胎顺利着床。
Objective: To investigate the role of activated β-catenin in embryo implantation. Methods: Kunming mice of the second day of gestation (d2) were randomly divided into 3 groups (30 rats in each group): group A: 0.1 ml mifepristone (1.2 mg / ml) Control): The same amount of 1,3-propanediol instead of mifepristone; C group: without any treatment. Immunohistochemistry, indirect immunofluorescence and Western blotting were used to detect the dynamic expression of β-catenin activated by d3 ~ 7 in three groups of mice at the same time. RESULTS: The activated β-catenin in endometrium of mice in group B and group C was expressed in the epithelium and luminal epithelium, stromal cytoplasm and cell membrane of the gland at the third trimester of pregnancy. The expression of d4 in the cytoplasm and cell membrane of the epithelial cells in pregnancy was strongly and reached the peak. There was no significant difference in the expression of d5 ~ 7 in the glandular epithelium, vascular endothelium, subepithelial stromal cell membrane and cytoplasm between groups B and C at all time points of d3 ~ 7 (P> 0.05) The expression of activated β-catenin in d3 ~ 7 group was significantly lower than that in group B and C (P <0.01). The expression of d3 ~ 7 in d4 was not peaked in d4, and the expression site was confined to stromal cells. CONCLUSION: Mifepristone may inhibit the progesterone binding to its receptor and down-regulate the expression of activated β-catenin, thereby inhibiting the adhesion of endometrium and affecting the establishment of endometrial receptivity, which hinders smooth embryo implantation.