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陈业文,胡元灏,程龙,刘俏,晏彪*,吴喆#. 过敏症状儿童室内PM2.5对小鼠巨噬细胞的氧化损伤及VE的抗氧化保护作用研究[J]. 生态毒理学报, 2018, 13(2): 120-127
过敏症状儿童室内PM2.5对小鼠巨噬细胞的氧化损伤及VE的抗氧化保护作用研究
Vitamin E Mitigates Indoor PM2.5-induced Oxidative Stress in Mouse Peritoneal Macrophages: Implication in Children Living with Allergy
投稿时间:2017-09-29  修订日期:2017-11-07
DOI:10.7524/AJE.1673-5897.20170929002
中文关键词:  室内PM2.5  巨噬细胞  氧化损伤  炎症因子  维生素E
英文关键词:indoor PM2.5  macrophages  oxidative damage  inflammatory factors  Vitamin E
基金项目:湖北科技学院校级资助项目(2016-18X026)
作者单位
陈业文,胡元灏,程龙,刘俏,晏彪*,吴喆# 湖北科技学院基础医学研究中心咸宁 437100 
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中文摘要:
      越来越多的研究提示,主要空气污染物PM2.5暴露浓度的升高与儿童过敏性疾病的发病率有着密切的关系,然而PM2.5暴露与过敏性疾病之间的关联尚未完全阐明。为探究患有过敏症状儿童的室内PM2.5对小鼠巨噬细胞的氧化损伤作用以及维生素E(vitamin E,VE)的抗氧化保护作用,从5户患有1种或1种以上的过敏性症状(如过敏性鼻炎、哮喘)儿童的室内采集PM2.5,分别考察了不同剂量PM2.5暴露24 h后如何影响小鼠巨噬细胞的氧化应激水平,指标包括活性氧(ROS),还原型谷胱甘肽(GSH),丙二醛(MDA),8-羟基脱氧鸟苷(8-OH-dG),以及炎症因子水平,指标包括肿瘤坏死因子ɑ(TNF-ɑ),白介素8β(IL-8β)的影响。结果表明,200 μg mL-1 PM2.5暴露组与对照组比较,细胞内ROS积累,出现脂质过氧化以及DNA损伤,并伴有炎症反应的发生,差异均有统计学意义(P< 0.05或P< 0.01);VE(50 mg mL-1)+ 200 μg mL-1 PM2.5组的ROS、MDA、8-OH-dG、TNF-ɑ、IL-8β含量低于200 μg mL-1 PM2.5组,GSH含量高于200 μg mL-1 PM2.5组。较高剂量(200 μg mL-1)PM2.5可诱导小鼠腹腔巨噬细胞出现氧化损伤,VE在该应激过程中起着一定的保护作用。
  
AuthorAffiliation
Chen Yewen, Hu Yuanhao, Cheng Long, Liu Qiao, Yan Biao*, Wu Zhe#Research Center of Basic Medical Sciences, Hubei University of Science and Technology, Xianning 437100, China
英文摘要:
      Inhalable fine aerosol particles, namely atmospheric particulate matter with a diameter of 2.5 μm or less (PM2.5), are well recognized as one of the major air pollutants that are harmful to human health. Previous studies have demonstrated that increased concentration of PM2.5 is closely related to the incidence of allergic diseases in children. However, the mechanisms by which PM2.5 exposure is associated to allergic diseases remain elusive. To study the role of oxidative stress and macrophages in PM2.5-induced damage in children living with allergy, we first sampled PM2.5 from five apartments, each housing one child or more who is manifested with at least one allergic symptom like allergic rhinitis or asthma. Mouse peritoneal macrophages were exposed to the collected PM2.5 (200 μg mL-1) for 24 h, with or without the addition of Vitamin E in the medium. Treated macrophages were subjected to detection of the levels of reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OH-dG) as oxidative markers, and tumor necrosis factor-ɑ (TNF-ɑ) and interleukin-8β (IL-8β) as inflammatory mediators. The results showed significant increase in intracellular ROS accumulation, lipid peroxidation, DNA damage and inflammatory response in macrophages exposed to 200 μg mL-1 PM2.5 as compared to control air exposure (P< 0.05 orP< 0.01). Interestingly, the levels of ROS, MDA, 8-OH-dG, TNF-ɑ and IL-8 in PM2.5-exposed macrophages were significantly lower, whereas that of GSH higher, in the presence than the absence of 50 mg mL-1 Vitamin E. These results indicate that a higher dose (200 μg mL-1) of PM2.5 leads to oxidative damage in mouse macrophages, and Vitamin E could mitigate the PM2.5-induced cellular oxidative stress, exhibiting implication in therapeutic treatment of allergy in children.
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