输卵管妊娠（TEP）滋养细胞上皮间质转化（EMT）而不断向输卵管侵袭是导致输卵管破裂的关键环节。课题组证实加味宫外孕I号方能抑制滋养细胞侵袭并使EMT上皮标志物E-cad生成增加，但机制不详。预实验发现，miR-184可调控靶基因EPB41L5翻译抑制TEP滋养细胞EMT，而该方能上调miR-184表达；生信分析预测UCA1与miR-184存在结合位点，且沉默UCA1靶基因EPB41L5蛋白表达呈下调趋势。因此，本研究拟进一步验证UCA1、miR-184及EPB41L5在TEP绒毛组织中的表达模式，制备UCA1过表达和敲除滋养细胞模型，应用siRNA/cDNA转染、双荧光素酶报告基因实验等技术，验证UCA1海绵吸附miR-184调控EPB41L5翻译在加味宫外孕I号方抑制TEP滋养细胞EMT中的作用及机制。此研究将为TEP发病机制及加味宫外孕I号方治疗TEP的作用靶点和机理探讨提供新思路。

Trophoblastic epithelial mesenchymal transformation (EMT) of tubal ectopic pregnancy (TEP) and continuous invasion to the fallopian tube is the key to the rupture of fallopian tube. Our previous study confirmed that Modified Gongwaiyun Formula I can inhibit the invasion of trophoblast and increase the production of E-cad, an epithelial marker of EMT, but the mechanism is unknown. In the pre experiment, we found miR-184 could regulate the translation of target gene EPB41L5 to inhibit the EMT of TEP trophoblasts, while this formula could up regulate the expression of miR-184; Bioinformatics analysis showed that there were binding sites between UCA1 and miR-184, while the silencing of UCA1 could down regulate the expression of target gene EPB41L5. Therefore, this study intends to further verify the expression of UCA1, miR-184 and EPB41L5 in TEP villi, prepare UCA1 overexpression and knockout trophoblast models, and use siRNA/cDNA transfection, dual luciferase reporter assay and some other technologies to verify the role and mechanism of UCA1 sponge adsorption miR-184 in regulating EPB41L5 translation in the inhibition of TEP trophoblast EMT by Modified Gongwaiyun Formula I. This study will provide a new idea for the pathogenesis of TEP and the mechanism and target study of Modified Gongwaiyun Formula I therapy for TEP.