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首页> 外文期刊>Mediators of inflammation >Simulating Sleep Apnea by Exposure to Intermittent Hypoxia Induces Inflammation in the Lung and Liver
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Simulating Sleep Apnea by Exposure to Intermittent Hypoxia Induces Inflammation in the Lung and Liver

机译：通过暴露于间歇性缺氧来模拟睡眠呼吸暂停诱导肺和肝脏炎症

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摘要

Sleep apnea is a breathing disorder that results from momentary and cyclic collapse of the upper airway, leading to intermittent hypoxia (IH). IH can lead to the formation of free radicals that increase oxidative stress, and this mechanism may explain the association between central sleep apnea and nonalcoholic steatohepatitis. We assessed the level of inflammation in the lung and liver tissue from animals subjected to intermittent hypoxia and simulated sleep apnea. A total of 12 C57BL/6 mice were divided into two groups and then exposed to IH (n = 6) or a simulated IH (SIH) (n = 6) for 35 days. We observed an increase in oxidative damage and other changes to endogenous antioxidant enzymes in mice exposed to IH. Specifically, the expression of multiple transcription factors, including hypoxia inducible factor (HIF-1alpha), nuclear factor kappa B (NF-kappaB), and tumor necrosis factor (TNF-alpha), inducible NO synthase (iNOS), vascular endothelial growth factor (VEGF), and cleaved caspase 3 were shown to be increased in the IH group. Overall, we found that exposure to intermittent hypoxia for 35 days by simulating sleep apnea leads to oxidative stress, inflammation, and increased activity of caspase 3 in the liver and lung.
机译：睡眠呼吸暂停是一种呼吸紊乱，由上呼吸道的瞬间和循环坍塌产生，导致间歇性缺氧（IH）。 IH可以导致形成增加氧化应激的自由基，并且这种机制可以解释中央睡眠呼吸暂停和非酒精脂肪肝炎之间的关联。我们评估了对受间歇性缺氧和模拟睡眠呼吸暂停的动物的肺和肝组织中炎症水平。将总共​​12个C57BL / 6小鼠分成两组，然后暴露于Ih（n = 6）或模拟的Ih（SiH）（n = 6）35天。我们观察到氧化损伤的增加和其他对暴露于IH的小鼠内源性抗氧化酶的变化。具体地说，多转录因子的表达，包括缺氧诱导因子（HIF-1α），核因子κB（NF-κB）和肿瘤坏死因子（TNF-α），诱导的无合成酶（INOS），血管内皮生长因子（VEGF），并且裂解的Caspase 3在IH组中被增加。总体而言，我们发现通过模拟睡眠呼吸暂停导致肝脏和肺中Caspase 3的氧化应激，炎症和增加的氧化应激，炎症和增加的活性暴露于间歇性缺氧35天。

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