Establishment and Evaluation of a Stable and Reliable Rat Model of Cesarean Scar Diverticulum

Cesarean scar diverticulum (CSD), a common complication of cesarean sections linked to poor uterine incision healing, has been hindered by the lack of standardized animal models. This study establishes a stable and reproducible CSD rat model, addressing this gap and providing a critical foundation for exploring pathological mechanisms and advancing therapies. The CSD model was established in 120 female rats (sham: 20; control/experimental: 50 each) via surgical resection and LPS injection. CSD formation was validated by B-mode/contrast-enhanced ultrasound. Histopathology (H&E, Masson's trichrome) quantified collagen deposition and neutrophil infiltration. Immunofluorescence (Collagen I, α-SMA) and immunohistochemistry (TNF-α, IL-6, iNOS) assessed fibrosis and inflammation. Quantitative analyses utilized confocal microscopy and ImageJ. Data were analyzed by SPSS 20.0. The LPS-induced CSD model showed higher detection rates (48% vs. 25%, p < 0.001), further enhanced by intrauterine saline (65% vs. 37.5%, p < 0.05) and SF6 contrast ultrasound (70% vs. 45%, p < 0.05). Histopathology revealed endometrial thinning, 250% neutrophil influx (p < 0.001), and elevated collagen deposition (p < 0.05). Fibrosis markers (Collagen I, α-SMA⁺ cells) and proinflammatory mediators (IL-6, TNF-α, iNOS) were significantly upregulated (p < 0.05), with CD68⁺ macrophages 3.2-fold higher in CSD lesions (p < 0.01). This study innovatively establishes a surgical-LPS-induced rat model of CSD that faithfully recapitulates clinical-pathological hallmarks, including characteristic endometrial-myometrial injury, fibrotic remodeling, and chronic inflammatory microenvironment. Overcoming limitations of conventional approaches, this model provides a standardized platform for unlocking pathogenesis and advancing targeted therapies for CSD.