Mandibular Advancement Attenuates Endmt Via Tgf-Β1 In Osa Rabbits

This study establishes an OSA and mandibular advancement (MAD) model in rabbits to investigate OSA-induced endothelial mesenchymal transition (EndMT) and its role in endothelial damage, while assessing MAD's potential to prevent EndMT, offering insights for clinical OSA therapy. Animal Model: 18 male New Zealand white rabbits (6-month-old) randomized into CON/OSA/MAD groups (n=6). OSA/MAD groups: palatal hyaluronate-induced airway obstruction; MAD group: mandibular appliances. All groups: daily chloral hydrate-induced supine sleep (2-4h) for 8 weeks. Assessments: Carotid structure: Ultrasound (CIMT), TEM (ultrastructure), Sirius red (fibrosis). EndMT: IHC/PCR/WB/ELISA for CD31, CDH1, FSP1, α-SMA. TGF-β1: PCR (mRNA) and ELISA (protein). Polysomnography: OSA group showed significantly higher AHI and lower SaO₂/LSaO₂ vs CON (P<0.05). MAD treatment improved these parameters (P<0.05). Carotid structure: Ultrasound: Increased CIMT in OSA vs CON; MAD prevented thickening (P<0.05) Sirius red: OSA showed severe fibrosis with ↑collagen I fibers vs CON/MAD (P<0.05) EM: Endothelial smooth muscle cells observed only in OSA group EndMT markers: ↓Endothelial (CD31, CDH1) and ↑mesenchymal (α-SMA, FSP1) markers in OSA vs CON (P<0.05) MAD reversed these changes (P<0.05) TGF-β1: OSA showed ↑expression vs CON; MAD reduced levels (P<0.05) OSA promotes EndMT by activating TGF-β1, leading to damage and dysfunction of common carotid artery endothelial structure. MAD treatment can effectively prevent the occurrence of these lesions.