Objective To investigate the mechanism by which yin-yang protein 1 (YY1) mediates the transformation growth factor beta (TGF-β) pathway in regulating fibrosis and mesenchymal transition of human fallopian tube inflammatory cells. Methods Using human fallopian tube epithelial cells as the object, a human fallopian tube epithelial cell inflammation model was established by intervention with lipopolysaccharide (LPS). Divided into LPS group, LPS+si NC group, LPS+si-YY1 group, and LPS+si-YY1+TGF-β group. Protein immunoblotting was used to detect the expression levels of YY1, anti-α-smooth muscle actin (α-SMA), N-cadherin, E-cadherin, and type I collagen in each group. Real time fluorescence quantitative PCR (RT-qPCR) was used to detect the expression of E-cadherin and compare the differences in fibrosis and mesenchymal transition indicators among the groups. Results The LPS si-NC group and the LPS si-YY1 group had comparable E-cadherin mRNA levels, with no statistically significant difference (P>0.05); for E-cadherin mRNA in the remaining groups, the levels were LPS group 0.05); the levels in the LPS si-YY1 group were lower than those in the LPS si-YY1 TGF-β group, which were lower than the LPS group. For E-cadherin protein, there was no statistically significant difference between the LPS si-YY1 group and the LPS si-NC group (P>0.05); the levels followed the order LPS si-YY1 group> LPS si-YY1 TGF-β group> LPS group, with all differences being statistically significant (P<0.05)。Conclusion YY1 can mediate the TGF-β pathway to regulate the fibrosis and mesenchymal transformation of tubal lumen and improve the outcome of tubal inflammatory infertility