中文摘要：

目的：研究健胎液对胚泡着床障碍小鼠着床期子宫内膜容受性的影响。方法：于妊娠第4天9：00利用米非司酮建立胚泡着床障碍小鼠模型，予健胎液进行干预，于妊娠第4天21：00处死小鼠，观察小鼠胚泡着床率及平均着床胚泡数，采用放免法检测血清及子宫组织雌二醇、孕酮的含量，采用逆转录聚合酶链式反应（RT-PCR）检测子宫ERmRNA、PRmRNA表达。结果：与模型组相比，中药组着床率和平均着床胚胎数均显著升高，与对照组无显著差异；模型组子宫内膜发育不良，中药组子宫内膜的发育与正常组相似；3组血清及子宫组织的雌二醇和孕酮的含量无显著改变；中药组子宫ERmRNA、PRmRNA表达均较模型组显著提高，与正常组比较差异无显著性。结论：健胎液通过促进子宫内膜发育，调节胚泡着床障碍小鼠子宫组织ER、PR基因的表达，改善子宫内膜容受性，利于胚泡着床。

英文摘要：

Objective： To in embryo implantation dysfun explore Effect of Jiantai Liquid （JTL）on endometrial receptivity during implantation ction mice（EID）. Method： Mice midel of EID induced by mifepristone at 9 AM on day 4 of pregnancy （Pd4） were intervened with JTL, and sacrificed at 9 PM on Pd4. Their uterine horns were examined for the presence of implanted embryos. Estradiol and progesterone concentrations in serum and endometrium tissue homogenate were measured by radioimmunoassay. The structure of endometrium was observed by light-microscope. Estradiol and progesterone concentrations in serum and endometrium tissue homogenates were measured by radioimmunoassay method, the endometrial expressions of ER mRNA and PR mRNA were assessed by semi-quantitative reverse transcriptase polymerase chain reaction （RT-PCR）. Result： The treatment implantation rate and average embryo number were significantly higher than that in experiment group, but there was no difference with control group. Endometrial morphology showed endometrial development retardation in model group, while endometrialdevelopmentin treatment groupwas significanflyimproved and neartysimilartocontrolgroup. There were no significantly differences in the estradioI and progesterone concentrations in serum and uterus tissue homogenates among three groups. Levels of ER mRNA and PR mRNA in the JTL treated group were significantly higher than those in the model group respectively, and showed insignificant differences from thoses in the normal control group. Conclusion： JTL could promote endometrial receptivity during implantation and improve the embryo implantation by way of regulate development of endometrium and the levels of ER and PR gene expression in mice with EID.