Chronic obstructive pulmonary disease (COPD), a respiratory disease characterized by inflammation due to neutrophil infiltration, has become the third leading cause of death worldwide. After the occurrence of COPD, the persistent accumulation of neutrophils can promote the excessive formation of neutrophil extracellular traps (NETs), which plays an important role in local capture and clearance of pathogens, rapid control of infection, and immune regulation. This article mainly introduces the mechanism of COPD occurrence and NETs formation as well as the research progress of NETs in COPD, and summarizes the relevant drug targets for COPD treatment based on NETs, aiming to provide a reference for further research.

Ischemic stroke, a cerebrovascular disease with high incidence, high mortality, high disability rate and high recurrence rate, is an important cause of death and disability of middle-aged and elderly people in China, and imposes a huge burden to society and families. Therefore, it is essential to identify the risk factors associated with ischemic stroke and effectively prevent them. Studies have shown that obstructive sleep apnea is an independent risk factor for ischemic stroke. However, the exact pathological mechanism of their association has not been clarified. With the development of next-generation sequencing technology, more and more studies have focused on intestinal microbiota. They have found that obstructive sleep apnea can cause intestinal microbiota changes, and intestinal microbiota may be closely related to ischemic stroke. Therefore, this paper attempts to investigate the relationship between intestinal flora and ischemic stroke, so as to reveal the potential pathological mechanism of ischemic stroke caused by obstructive sleep apnea.

阻塞性睡眠呼吸暂停综合征(OSAS)是一种多发的临床疾病,常并发多种器官损伤.炎症反应在OSAS及其并发症的发生发展过程中发挥重要作用.Toll样受体(TLRs)是模式识别受体(PRRs),可特异地识别病原体相关分子模式(PAMP),导致细胞内信号转导通路的活化,促进体内炎症介质的释放(CRP、IL-6、TNF-α和IFN-γ等),激活免疫炎性反应.TLRs在OSAS及其并发症患者组织细胞中异常表达,可以通过TLR/MyD88通路促进软腭血管生成、扁桃体肥大等参与OSAS的发生发展;还能够通过损害海马神经元自噬功能等损伤OSAS患者认知功能;通过损伤内皮细胞、刺激泡沫细胞形成等参与OSAS并发心血管损伤的发生发展;通过诱导肾促炎巨噬细胞和成纤维细胞募集等参与OSAS并发肾损伤的发生发展;通过促进炎症因子增多、干扰Treg/Th17平衡等参与OSAS并发肝损伤的发生发展;通过改变肺泡形态及功能等参与OSAS并发肺损伤的发生发展;通过诱导胰岛素抵抗等参与OSAS并发代谢异常的发生发展.

为应对日益增强的内源性和外源性氧化损伤因子,哺乳动物的细胞防御机制处于不断进化过程中.近年来,随着相关研究不断深入,核因子E2相关因子2(Nrf2)被誉为抗氧化损伤的"明星"分子,国际上耗费数百亿美元来开发相关靶向激活或抑制剂.阻塞性睡眠呼吸暂停(OSA)是临床上最常见的睡眠呼吸障碍形式,氧化应激是其最主要的病理机制之一,并与OSA心、脑、肺、肾等各系统靶器官损害密切相关.最近的研究揭示了Nrf2通路在OSA并发症中的机制联系,一些天然的Nrf2激活剂也通过动物实验展现出了新兴的治疗作用.然而,Nrf2在OSA不同靶器官的激活方式和效应途径尚未理清.因此,本文对Nrf2通路在OSA及其并发症的研究进展作一综述,以加深对OSA并发症机制的理解并提供一种潜在的治疗策略.

阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome, OSAHS)是常见的易引起多系统损害的一种呼吸系统疾病,主要因睡眠时上气道反复塌陷、阻塞、狭窄等引起气流减少或者停止,导致睡眠结构紊乱、间歇性低氧、炎性反应等病理生理变化[1] .