氧化应激
医学
免疫学
炎症
屋尘螨
哮喘
活性氧
卵清蛋白
药理学
化学
过敏
过敏原
内分泌学
免疫系统
生物化学
作者
R Chandrasekaran,S. Bruno,Z. Mark,Joseph Walzer,S. Caffry,Clarissa Gold,Amit Kumar,Nicolas Chamberlain,Isabella M. Butzirus,Carolyn R. Morris,Nirav Daphtary,Minara Aliyeva,Ying‐Wai Lam,Albert van der Vliet,Yvonne Janssen‐Heininger,Matthew E. Poynter,Anne E. Dixon,Vikas Anathy
出处
期刊:American Journal of Physiology-lung Cellular and Molecular Physiology
[American Physiological Society]
日期:2022-12-13
卷期号:324 (2): L141-L153
被引量:9
标识
DOI:10.1152/ajplung.00249.2022
摘要
Obesity is associated with severe, difficult-to-control asthma, and increased airway oxidative stress. Mitochondrial reactive oxygen species (mROS) are an important source of oxidative stress in asthma, leading us to hypothesize that targeting mROS in obese allergic asthma might be an effective treatment. Using a mouse model of house dust mite (HDM)-induced allergic airway disease in mice fed a low- (LFD) or high-fat diet (HFD), and the mitochondrial antioxidant MitoQuinone (MitoQ), we investigated the effects of obesity and ROS on HDM-induced airway inflammation, remodeling, and airway hyperresponsiveness (AHR). Obese allergic mice showed increased lung tissue eotaxin, airway tissue eosinophilia, and AHR compared with lean allergic mice. MitoQ reduced airway inflammation, remodeling, and hyperreactivity in both lean and obese allergic mice, and tissue eosinophilia in obese-allergic mice. Similar effects were observed with decyl triphosphonium (dTPP
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