〔Abstract〕 Objective To explore the mechanism of mesenchymal epithelial transformation(EMT) mediated by Wnt/β-catenin signaling pathway in the inhibition of endometrial fibrosis by endometrial mesenchymal stem cells(eMSCs). Methods Eighteen female SD rats were randomly divided into Sham group, Model group and eMSCs group, with 6 rats in each group. Rats in Sham group merely had laparotomy without any treatment. A rat model of intrauterine adhesion(IUA) was established in the Model group and eMSCs group. In eMSCs group, the total amount of eMSCs cell suspension transplanted immediately after model injury was 0.05 ml(2×107cells/ml) per uterus for treatment. Three weeks later, the uterus with unilateral injury was collected for hematoxylin-eosin(HE) staining and Masson staining. Endometrial fibrosis, EMT, Wnt/β-catenin pathway protein expression were analyzed by protein blot. Results In the Model group, the structure of the uterine cavity was destroyed and the number of glands were significantly reduced with a large number of blue collagen fibers were accumulated. However, after eMSCs treatment, the number of endometrial glands increased, and the fibrotic area decreased significantly. Compared with Sham group, the expression levels of type I collagen and α-SMA protein in Model group increased significantly(P<0.05), but decreased significantly in eMSCs group(P<0.05). In the Model group, the expressions of N-cadherin, vimentin and ZEB1 increased significantly, while the expression of E-cadherin decreased. However, in eMSCs group, the changes of protein of the above molecules were completely opposite. Compared with Sham group, the expression of β-catenin and C-myc increased in Model group(P<0.05). Compared with the Model group, the expressions of CyclinE, β-catenin and C-myc increased in eMSCs group(P<0.05). Conclusion eMSCs can promote endometrial repair in IUA rats by inhibiting EMT and endometrial fibrosis, which is partly achieved by activating Wnt/β-catenin signaling pathway.