目的:观察安坤种子丸对胚泡着床障碍小鼠血清雌、孕激素影响,探讨其对胚泡着床障碍小鼠子宫内膜容受性的影响及其机制。方法:将有规律动情周期的雌性小鼠随机分为正常组、模型组和中药组,每组25只。先用安坤种子丸对中药组小鼠进行灌胃,雌、雄合笼后观察雌鼠阴栓情况,之后各组选取有阴栓者20只并计为妊娠第1天(D1),雄鼠及其余雌鼠剔除。妊娠第4天对中药组和模型组小鼠颈背部皮下注射米非司酮,制成胚泡着床障碍模型;于妊娠第5、6天处死小鼠,留取血清标本。采用放射免疫法检测血清雌激素(E_2)和孕激素(P)的含量;同时制备HE切片以观察各组小鼠子宫内膜形态结构的变化,分析并统计观察各组平均着床胚泡数的变化。结果:安坤种子丸可以提高胚泡着床障碍小鼠血清E_2、P水平,中药组平均着床胚泡数虽低于正常组,但显著高于模型组,差异均有统计学意义(P<0.01)。结论:安坤种子丸可以通过提高雌鼠血清E_2、P水平,一定程度上改善着床障碍小鼠子宫内膜容受性,促进胚泡着床。 Objective: To observe the effect of Ankun seed pill on serum estradiol and progesterone in mice with blastocyst implantation dysfunction and to explore its effect on endometrial receptivity in mice with blastocyst implantation dysfunction and its mechanism. Methods: Female mice with regular estrous cycle were randomly divided into normal group, model group and TCM group, with 25 rats in each group. First, with the Ankun seed pill on the Chinese medicine group mice gavage, female and male cages were observed after the female rat suppository, after each group selected 20 patients with a negative suppository and accounted for the first day of pregnancy (D1), male Rats and other female rats removed. On the 4th day of gestation, mifepristone was subcutaneously injected into the back of the neck of mice in the model group and the model group. The embryo implantation dysfunction model was made. On the 5th and 5th day of gestation, the mice were sacrificed and the serum samples were collected. The levels of serum estrogen (E2) and progesterone (P) were measured by radioimmunoassay. HE slices were also prepared to observe the morphological changes of endometrium of mice in each group. The mean number of blastocysts in each group The change. Results: Ankun seed pills can improve the levels of serum E_2 and P in mice with blastocyst implantation disorder. Although the mean number of blastocyst in Chinese medicine group is lower than that in normal group, it is significantly higher than that in model group (P <0.01). Conclusion: Ankun seed pills can improve endometrial receptivity and promote implantation of blastocyst in mice with dysplasia by increasing serum E_2 and P levels in female rats.