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氧化应激在支气管哮喘发病机制中的参与作用。

The participation of oxidative stress in the pathogenesis of bronchial asthma.

机构信息

Department of Immunopathology, Faculty of Biomedical Sciences and Postgraduate Training, Medical University of Lodz, 7/9 Zeligowskiego St, bldg 2 Rm 122, 90-752 Lodz, Poland.

Department of Immunopathology, Faculty of Biomedical Sciences and Postgraduate Training, Medical University of Lodz, 7/9 Zeligowskiego St, bldg 2 Rm 122, 90-752 Lodz, Poland.

出版信息

Biomed Pharmacother. 2017 Oct;94:100-108. doi: 10.1016/j.biopha.2017.07.066. Epub 2017 Jul 27.

Abstract

Reactive oxygen species are produced during oxygen reduction and are characterized by high reactivity. They participate in many important physiological processes, but if produced in high concentrations they lead to oxidative stress development and disturb pro-oxidative/anti-oxidative balance towards the oxidation reaction - leading to damage of lipids, proteins, carbohydrates or nucleic acids. Asthma is a chronic inflammatory disease of the airways of various pathogenesis and clinical symptoms, prevalence in recent years has increased significantly. Recently published literature point out the involvement of reactive oxygen species in the pathogenesis of asthma. Changes in the protein and lipid oxidation lead, among others, to pathological changes in the respiratory epithelial cells, an increase in vascular permeability, mucus overproduction, smooth muscle contraction or airway hyperresponsiveness (AHR). The aim of this study is to present the current state of knowledge on the influence of oxidative stress parameters on asthma development.

摘要

活性氧在氧还原过程中产生,具有高反应性。它们参与许多重要的生理过程,但如果产生的浓度过高,会导致氧化应激的发展,并破坏氧化反应的促氧化/抗氧化平衡——导致脂质、蛋白质、碳水化合物或核酸的损伤。哮喘是一种气道的慢性炎症性疾病,具有多种发病机制和临床症状,近年来其患病率显著增加。最近发表的文献指出,活性氧参与了哮喘的发病机制。蛋白质和脂质氧化的变化,除其他外,导致呼吸道上皮细胞的病理变化、血管通透性增加、黏液过度产生、平滑肌收缩或气道高反应性(AHR)。本研究旨在介绍氧化应激参数对哮喘发展影响的最新知识状况。

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