Dulaglutide Ameliorates Intrauterine Adhesion by Suppressing Inflammation and Epithelial–Mesenchymal Transition Via Inhibiting the TGF-β/Smad2 Signaling Pathway

Intrauterine adhesion (IUA) is a common gynecological disease with limited therapeutic options. Dulaglutide long-acting glucagon-like peptide-1 (GLP-1) analog some anti-fibrotic and anti-inflammatory properties; however, its action on IUA remains uncertain. The purpose of the experiments in this study was to explore effect dulaglutide elucidate mechanism provide new ideas for clinical treatment IUA. An mouse model established via mechanical curettage inflammation induction; mice received subcutaneous injection three doses once day two weeks (treatment) or equal amounts sterile ddH2O (control), sham-operated were treated similarly control mice. Mice sacrificed, uterine tissues subjected hematoxylin eosin (H&E) Masson’s trichrome staining histomorphological pathological analyses real-time quantitative polymerase chain reaction (RT-qPCR) Western blotting (WB) gene protein expression analyses. improved shape cavity, increased endometrial thickness number glands, significantly reduced area collagen fiber deposition endometrium. It type I A 1 (COL1A1), interleukin-1beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), C-C motif chemokine ligand 2 (CCL2), F4/80 (macrophage), vimentin transforming growth factor-beta (TGF-β) mRNA levels COL1A1, IL-1β, IL-6, TNF-α, F4/80, vimentin, E-cadherin, TGF-β, p-Smad2 levels. This demonstrates that reduces inflammatory responses by inhibiting M1 macrophage polarization factor release may ameliorate fibrosis epithelial–mesenchymal transition (EMT) TGF-β/Smad2 signaling.