在阻塞性睡眠呼吸暂停综合征中,通过间歇性缺氧选择性激活炎症通路
Silke Ryan1, Cormac T Taylor, Walter T McNicholas
1Sleep Research Laboratory, St Vincent's University Hospital, Dublin, Ireland.
Circulation
|October 26, 2005
概括
阻塞性睡眠呼吸暂停综合征 (OSAS) 激活炎症通路,而不是适应性通路,在间歇性缺氧/低氧化 (IHR). 这种选择性炎症可能会导致OSAS患者的心血管疾病.
科学领域:
- 心血管疾病研究研究
- 睡眠医学 睡眠医学
- 分子生物学分子生物学
背景情况:
- 阻塞性睡眠呼吸暂停综合征 (OSAS) 是心血管疾病的重要危险因素,与间歇性缺氧/低氧化 (IHR) 有关.
- 连接OSAS和心血管并发症的精确分子机制需要进一步阐明.
研究的目的:
- 调查OSAS与心血管疾病之间的关联背后的分子机制.
- 在转化模型中检查IHR响应的炎症和适应途径的激活.
主要方法:
- 利用暴露于IHR的体外HeLa细胞模型,使用记者结构和DNA结合试验来研究NF-kappaB和HIF-1.
- 对男性OSAS患者和匹配的对照进行了前性研究,测量了循环瘤坏死因子-alpha,红色素,中性粒细胞水平和血红素.
- 在持续的正气道压力 (CPAP) 治疗6周后,评估了OSAS患者的变化.
主要成果:
- 在体外IHR选择性地激活了促炎转录因子NF-kappaB,而适应性调节器HIF-1保持不活跃.
- 与对照组相比,OSAS患者表现出更高的循环水平的促炎性细胞因子瘤缩因子-α和中性粒细胞计数.
- 在OSAS患者中,CPAP疗法使瘤亡因子-α水平正常化,而红色素水平和血红素水平保持不变.
结论:
- 该研究表明,在IHR和OSAS期间,炎症通路选择性激活,而不是适应性通路.
- 这种有利于炎症的不平衡被认为是导致OSAS心血管疾病的关键分子机制.
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