ArticleNature and science of sleep2025
Impact of Obstructive Sleep Apnea on Endometrial Function in Female Rats: Mechanism Exploration.
Article in Nature and science of sleep, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Elevated systemic oxidative stress contributes to endometrial damage. Individuals with obstructive sleep apnea (OSA) exhibit significantly elevated oxidative stress; however, the potential role of oxidative stress in OSA-induced endometrial injury remains unclear. Objective: To investigate the effects of OSA on systemic oxidative stress and endometrial morphological alterations in a female rat model. Methods: We randomly assigned 15 female Sprague-Dawley (SD) rats to three groups: (1) Control group: Normal feeding for 8 weeks; (2) Short-term OSA group: 4 weeks of normal feeding followed by 4 weeks of Sleep Apnea (SA) modeling; (3) Long-term OSA group: 8 weeks of SA modeling.Assessments included: Body weight; uterine index; Oxidative stress markers: superoxide dismutase (SOD), reactive oxygen species (ROS) and malondialdehyde (MDA);Endometrial histomorphology: thickness, microvessel density and gland count via Hematoxylin and Eosin (H&E) staining; immunohistochemical (IHC) analysis of Kiel 67 (Ki-67) antigen and vascular endothelial growth factor (VEGF); Apoptosis detection by terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) assay. Results: Long-term OSA exposure significantly increased body weight vs control (P<0.05). Both OSA groups showed reduced uterine indices and elevated oxidative stress (P<0.05). Progressive structural impairment was observed with OSA duration: endometrial thickness and microvessel density decreased sequentially (control > short-term > long-term; P<0.05), and gland number was reduced in the long-term group vs control (P<0.05). IHC showed duration-dependent suppression of Ki-67 (proliferation) and VEGF (angiogenesis) expression (P<0.05), while apoptosis increased with OSA exposure (P<0.05). Conclusion: In a preclinical model, OSA-like exposure promoted weight gain, uterine atrophy, and progressive endometrial damage. Mechanistic analyses revealed that this impairment resulted from oxidative stress-mediated inhibition of cellular proliferation (reflected by reduced Ki-67 expression) and suppression of angiogenesis (indicated by decreased VEGF levels), concurrent with enhanced apoptotic activity. Given the observed duration-dependent pathological progression, our findings establish that sleep apnea contributes to female reproductive dysfunction, warranting early clinical intervention in women with sleep-disordered breathing.
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