Nature and science of sleep · 2025
Impact of Obstructive Sleep Apnea on Endometrial Function in Female Rats: Mechanism Exploration.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Zhang Dong, Bian Wenli, Gao Zhihua
Аннотация
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.
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.