缺氧(环境)
软腭
病理
间歇性缺氧
医学
H&E染色
发病机制
解剖
免疫组织化学
阻塞性睡眠呼吸暂停
内科学
化学
外科
有机化学
氧气
作者
Cong Liu,Yu Zhang,Yuqin Chen,Tianning Su,Yang Zhao,Song Shi
出处
期刊:Medical Science Monitor
[International Scientific Information, Inc.]
日期:2020-05-11
卷期号:26
被引量:4
摘要
BACKGROUND:Chronic intermittent hypoxia (CIH) is a key feature of obstructive sleep apnea (OSA) syndrome. The pathogenesis of CIH-induced soft palate lesion is not well understood. Understanding the mechanisms of CIH-induced soft palate damage could provide new strategies for clinical treatment. MATERIAL AND METHODS:Twenty male Sprague‑Dawley rats were randomized into a control group (n=10) and experimental group (n=10). The experimental group were exposed to CIH for 28 days. The control experiments were run in parallel. Morphological changes of CIH-induced soft palate were examined by hematoxylin and eosin. Peripheral nerves and vascular associated markers were analyzed by western blot and immunohistochemical staining. LC3B expression and transmission electron microscopy analysis was detected to investigate the destiny of cells in CIH-induced soft palate. RESULTS:Histological studies demonstrated the thicken mucosal layer, muscular changes consistent with glands hyperplasia, and loose connective tissues of the soft palate in CIH induced rat models. CIH exposure significantly decreased the expression of annexin V but did not change argin level, suggesting that sensory nerves not motor nerves were damaged when exposed to intermittent hypoxia. Moreover, in response to CIH, the vascular vessel around the nerves and muscles became enlarged and caveolin-1 was overexpressed. Autophagy occurs in response to CIH-induced neuromuscular and vascular endothelial injury. CONCLUSIONS:Sensory nerves and endothelial dysfunction contributed to the morphological damage of soft palate under intermittent hypoxia. Autophagy as a compensatory mechanism protects against CIH-induced injury. These findings have important implications for understanding mechanisms contributing to the increased soft palate lesion in patients with OSA.
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