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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 被引量:5

The Effects of Acute and Chronic Ozone Exposure on Inflammation,Structure and Function in Murine Lung
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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。 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.
出处 《中国呼吸与危重监护杂志》 CAS 2014年第3期295-299,共5页 Chinese Journal of Respiratory and Critical Care Medicine
基金 国家自然科学基金(编号:81100024) 上海市卫生局局级课题(编号:2011247)
关键词 臭氧 肺部炎症 肺部结构 肺功能 Ozone Lung inflammation Lung structure Lung function
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参考文献14

  • 1Ko FW, Tam W, Wong TW, et al. Effects of air pollution on asthma hospitalization rates in different age groups in Hong Kong. Clin Exp Allergy, 2007,37 : 1312-1319.
  • 2Medina-Ramon MA, Zanobetti A, Schwartz J. The effect of ozone and PM10 on hospital admissions for pneumonia and chronic obstructive pulmonary disease: a national multicity study. Am J Epidemiol, 2006,163:579-588.
  • 3Mudway IS, Kelly FJ. An investigation of inhaled ozone dose and the magnitude of airway inflammation in healthy adults. Am J Respir Crit Care Med ,2004, 169 : 1089-1095.
  • 4Alexeeff SE, Litonjua AA, Wright RO, et al. Ozone exposure, antioxidant genes, and lung function in an elderly cohort: VA normative aging study. Oecup Environ Med ,2008,65:736-742.
  • 5Que LG, Stiles JV, Sundy JS, et al. Pulmonary function, bronchial reactivity, and epithelial permeability are response phenotypes to ozone and develop differentially in healthy humans. J Appl Physiol, 2011,111:679-687.
  • 6Yang W, Omaye ST. Air pollutants, oxidative stress and human health. Mutat Res ,2009,674:45-54.
  • 7李锋,张旻,周新.氧化应激与慢性气道疾病[J].中国呼吸与危重监护杂志,2012,11(1):97-100. 被引量:6
  • 8Chung KF, Adcock IM. Multifaceted mechanisms in COPD: inflammation, immunity, and tissue repair and destruction. Eur Respir J,2008,31 : 1334-1356.
  • 9Li F, Wiegman C, Seiffert J, et al. Effects of N-acetylcysteine in ozone-induced chronic obstructive pulmonary disease model. PLoS ONE,2013,8 : e80782.
  • 10Johnson KA. Imaging techniques for small animal imaging models of pulmonary disease : micro-CT. Toxicol Patho1,2007,35:59-64.

二级参考文献29

  • 1Masoli M, Fabian D, Holt S, et al. The global burden of asthma:executive summary of the GINA Dissemination Committee report. Allergy, 2004,59 : 469 -478.
  • 2Yao H, de Boer WI, Rahman I. Targeting lung inflammation : novel therapies for the treatment of COPD. Curr Respir Med Rev ,2008,4 : 57-68.
  • 3Lee W,Thomas PS. Oxidative stress in COPD and its measurement through exhaled breath condensate. Clin Transl Sci, 2009,2 : 150- 155.
  • 4Comhair SA, Erzumm SC. Antioxidant response to oxidant-mediated lung disease. Am J Phyisol Lung Cell Mol Phyiso1,2002,283 :L246- L255.
  • 5Tsukagoshi H, Kawata T, Shimizu Y, et al. 4-Hydroxy-2-nonenal enhances fibronectin production by IMR-90 human lung fibroblasts partly via activation of epidermal growth factor receptor-linked extracellular signal-regulated kinase p44/42 pathway. Toxicol Appl Pharmacol, 2002,184 : 127-135.
  • 6Williams AS, Issa R, Leung SY, et al. Attenuation of ozone-induced airway inflammation and hyperresponsiveness by c-Jun NH2 terminal kinase inhibitor SP600125. J Pharmacol Exp Ther, 2007, 322:351-359.
  • 7Williams AS, Issa R, Durham A, et al. Role of p38 mitogen-activated protein kinase in ozone-induced airwayhyperresponsiveness and inflammation. Eur J Pharmaco1,2008,600 : 117-122.
  • 8Marwick JA ,Caramori G, Casolari P, et al. A role for PI3Kdeha in the impairment of glucocorticoid responsiveness in COPD. JAller Clin Immunol,2010,125 : 1146-1153.
  • 9Dagher Z, Garcon G, Billet S, et al. Role of nuclear factor-kappa B activation in the adverse effects induced by air pollution particulate matter ( PM2.5 ) in human epithelial lung cells (L132) in culture. J Appl Toxicol,2007 ,27 :284-290.
  • 10Kensler TW, Wakabayashi N, Biswal S. Cell survival responses to environmental stresses via the Keapl-Nrf2-ARE pathway. Annu Rev Pharmacol Toxico1,2007,47:89-116.

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