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急性、慢性臭氧暴露对小鼠肺部炎症、肺部结构和肺功能的影响
引用本文:李锋,张鹏宇,张旻,包爱华,陈宇清,唐月琴,周新.急性、慢性臭氧暴露对小鼠肺部炎症、肺部结构和肺功能的影响[J].中国呼吸与危重监护杂志,2014(3):295-299.
作者姓名:李锋  张鹏宇  张旻  包爱华  陈宇清  唐月琴  周新
作者单位:上海交通大学附属第一人民医院呼吸科,上海200080
基金项目:国家自然科学基金( 编号: 81100024) ; 上海市卫生局局级课题( 编号: 2011247)
摘    要:目的 探讨急性、慢性臭氧暴露对小鼠肺部炎症、肺部结构和肺功能的影响。方法 32 只C57/BL6小鼠随机分为单次( 急性) 臭氧暴露组、单次空气暴露组、多次( 慢性) 臭氧暴露组( 1 次/3 d, 6 周) 和多次空气暴露组, 每组8 只。小鼠暴露于2. 5 ppm的臭氧环境中, 3 h/ 次。于臭氧暴露结束后24 h, 评估肺容积和低密度区( LAA) 比例、肺功能、支气管肺泡灌洗液( BALF) 细胞计数、BALF 丙二醛( MDA) 、血清8-脱氧鸟苷( 8-OHdG) 、肺部炎症积分以及肺组织平均内衬间隔( Lm) 。结果 与单次空气暴露组比较, 单次( 急性) 臭氧暴露增加BALF炎症细胞总数, 增加肺部炎症积分,增加BALF 中MDA 水平、血清8-OHdG 水平, 不影响肺容积、肺容积中LAA 比例、肺总量、呼吸气流、肺部Lm。与单次( 急性) 臭氧暴露组、单次空气暴露组、多次空气暴露组比较, 多次( 慢性) 臭氧暴露增加BALF 炎症细胞总数, 增加肺容积、肺容积中LAA 比例, 增加肺总量, 介导呼出气流阻塞, 增加肺部炎症积分和Lm。结论 急性臭氧暴露诱导气道/ 肺部炎症和氧化应激, 慢性臭氧暴露诱导气道/ 肺部炎症、肺气肿和呼出气流阻塞。

关 键 词:臭氧  肺部炎症  肺部结构  肺功能

The Effects of Acute and Chronic Ozone Exposure on Inflammation,Structure and Function inMurine Lung
Li Feng,Zhang Pengyu,Zhang Min,Bao Aihua,Chen Yuqing,Tang Yueqin,Zhou Xin.The Effects of Acute and Chronic Ozone Exposure on Inflammation,Structure and Function inMurine Lung[J].Chinese Journal of Respiratory and Critical Care Medicine,2014(3):295-299.
Authors:Li Feng  Zhang Pengyu  Zhang Min  Bao Aihua  Chen Yuqing  Tang Yueqin  Zhou Xin
Institution:.(Department of Respiratory Medicine, Shanghai First People’s Hospital, Shanghai Jiao Tong University,Shanghai, 200080, China)
Abstract:Objective To investigate the effects of acute and chronic ozone exposure oninflammation, structure and function in murine lung.Methods 32 C57/BL6 mice were randomly dividedinto a single ( acute) ozone exposed group, a single air exposed group, a multiple ( chronic) ozone exposedgroup ( every three days over 6 weeks) , and a multiple air exposed group with 8 mice in each group. Themice were exposed to 2.5 ppmof ozone or air for 3 hours per time and sacrificed 24 hours after the last timeof ozone exposure. Lung volume, low attenuation area ( LAA) percentage, lung function, cell counts andmalondialdehyde ( MDA) in bronchoalveolar lavage fluid ( BALF) , 8-hydroxy-2′-deoxyguanosine ( 8-OHdG)in serum, inflammation scores and mean linear intercept ( Lm) in lung section were assessed.Results Compared with the single air exposed group, single ( acute) ozone exposure led to increases in inflammatorycells in BALF, inflammation scores in the lung tissue,MDA in BALF and 8-OHdG in serum, but had no effecton lung volume, LAA percentage, airflow or Lm. Compared with the single ( acute) ozone exposed group, thesingle air exposed group and the multiple air exposed group, multiple ( chronic) ozone exposure increasedinflammatory cells in BALF, lung volume, LAA percentage, total lung capacity and lung compliance, mediatedairflow obstruction, and also increased lung inflammation socres and Lm.Conclusion Acute ozone exposureinduced airway/ lung inflammation and oxidative stress, while chronic ozone exposure induced airway/lunginflammation, emphysema and airflow obstruction.
Keywords:Ozone  Lung inflammation  Lung structure  Lung function
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