期刊文献+

吸烟所致肺气肿模型大鼠戒烟后肺病理及炎性介质的变化 被引量:8

The lung pathology changes and the expression of inflammatory mediators in smoking induced rats of emphysema model after smoking cessation
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摘要 目的探讨吸烟所致肺气肿模型大鼠在戒烟后肺组织病理及炎性介质表达变化规律。方法选用Wistar雄性大鼠80只,随机分为非吸烟正常对照组及吸烟所致肺气肿模型戒烟0 d、1 w、2 w、4 w、6 w、8 w、12 w组。采用酶联免疫吸附方法测定各组大鼠血清中IL-8的蛋白质含量,S-P免疫组化学方法检测肺组织NF-κB p65的表达,并光镜观察HE染色切片、对大鼠气道炎症进行病理学评分。结果肺气肿大鼠模型成功复制:肺组织HE染色切片,光镜下观察,其病理变化与人类肺气肿相似;肺气肿各时相戒烟组大鼠血清IL-8浓度、肺组织NF-κB的表达及病理评分较未吸烟正常对照组明显升高(P<0.05);肺气肿各相邻时相戒烟组间比较,各检测指标有上升趋势,戒烟12 w组大鼠血清中IL-8的蛋白质含量、肺组织NF-κB p65的表达、气道炎症的病理学评分均较戒烟0天组明显升高(P<0.05)。结论吸烟所致肺气肿模型大鼠形成后,其气道炎症在戒烟后12周内仍可见持续加重。 Objective To investigate the lung pathology changes and the expression of inflammatory mediators in smoking induced rats of emphysema model after smoking cessation.Methods 80 Wistar male rats were randomly divided into control and smoking induced emphysema model groups on the smoking cessation stage 0 day,1,2,4,6,8 and 12 weeks.Levels of IL-8 in serum was detected by ELISA,expression of NF-κB p65 in lung tissue was detected by S-P immunohistochemistry,and pathology score of inflammation on airway was carried out by observing HE stained lung tissue sections under light microscope.Results Rats of emphysema model was successful replicated: the pathological changes were similar to human emphysema by observing HE stained lung tissue sections under light microscope.Levels of IL-8 in serum,expression of NF-κB and pathological score in lung tissue of all emphysema model groups on any smoking cessation stage were significantly higher than those of non-smoking control group(P0.05).All indexes between adjacent stage emphysema groups had an upward trend.Levels of IL-8 in serum,expression of NF-κB and airway inflammation pathological score of groups on smoking cessation stage 12 weeks were significantly higher than those of groups on smoking cessation stage 0 days(P0.05).Conclusions After the rats of emphysema model is formed,their airway inflammation is still visible and continue to increase after 12 weeks smoking cessation.
出处 《中国老年学杂志》 CAS CSCD 北大核心 2011年第16期3080-3082,共3页 Chinese Journal of Gerontology
基金 辽宁省自然科学基金资助项目(20092103)
关键词 戒烟 肺气肿 炎性反应 Smoking cessation Emphysema Inflammatory response
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参考文献11

  • 1Asia Pacific COPD Roundtable Group. Global Initiative for Chronic Obstructive Lung Disease strategy for the diagnosis, management and prevention of chronic obstructive pulmonary disease : an Asia-Pacific perspective [J]. Respirology,2005 ;10(1 ) :9-17.
  • 2Rutgers SR, Postma DS,Ten Hacken NH,et al. Ongoing airway inflammation in patients with COPD who do not currently smoke[ J]. Chest ,2000 ; 117(5 supppl1) :262S.
  • 3Gamble E, Grootendorst DC, Hattotuwa K, et al. Airway mucosal inflammation in COPD is similar in smokers and ex-smokers:a pooled analysis [ J].Eur Respir J,2007 ;30 (3) :467-71.
  • 4Willemse BW,ten Hacken NH, Rutgers B,et al. Effect of 1-year smoking cessation on airway inflammation in COPD and asymptomatic smokers [ J]. Eur Respir J,2005 ;26(5 ) :835-45.
  • 5Vemooy JH, Dentener MA, van Suylen R J, et al. Long-term intrabrancheal lipopolysaccharide exposure in mice results in chronic lung inflammation and persistent pathology[ J]. Am J Respir Cell Mol Biol, 2002;26 (1) : 152-9.
  • 6Godtfredsen NS, Lam TH, Hansel TT, et al. COPD-related morbidity and mortality after smoking cessation: status of the evidence [ J ]. Eur Respir J,2008 ;32(4) :844-53.
  • 7Yao H, Edirisinghe I, Rajendrasozhan S, et al. Cigarette smoke-mediated inflammatory and oxidative responses are strain-dependent in mice [J]. Am J Physiol Lung Cell Mol Physio1,2008 ;294 ( 6 ) : L1174-86.
  • 8Culpitt SV, Rogers DF, Shah P, et al. Impaired inhibition by dexamethasone of cytokine release by alveolar macrophages from patients with chronic obstructive pulmonary disease[ J]. Am J Respir Crit Care Med,2003; 167( 1 ) :24-31.
  • 9Noguera A, Batle S, Miralles C, et al. Enhanced neutrophil response in chronic obstructive pulmonary disease [ J]. Thorax,2001 ;56 (6) :432-7.
  • 10Nishikawa M. Cigarette smoke-induced acute airway impairment [J].Nihon Kokyuki Gakkai Zasshi ,2000 ;38 (5) :347-53.

同被引文献60

  • 1李有仓.长期吸烟者的肺气肿和肺功能损害特征[J].中国临床康复,2004,8(33):7393-7395. 被引量:11
  • 2张陵,万宁.氧自由基脂质过氧化反应所致运动性疲劳产生机制研究进展[J].中国实验诊断学,2006,10(9):1104-1108. 被引量:20
  • 3薄其付,李若葆,王金平,李洪先.被动吸烟对大鼠肺泡上皮细胞结构及p53,K-ras表达的影响[J].潍坊医学院学报,2007,29(2):101-103. 被引量:11
  • 4Bafadhel M, Umar I, Gupta S, et al. The role of CT scanning in multidimensional phenotyping of COPD [J]. Chest, 2011, 140 (3) :634-642.
  • 5Johannessen A, Skorge TD, Bottai M, et al. Mortality by level of emphysema and airway wall thickness [ J ]. Am J Respir Crit Care Med, 2013, 187(6) :602-608.
  • 6Kohansal R, Martinez-Camblor P, Agusti A, et al. The natural his- tory of chronic airflow obstruction revisited : an analysis of the Fram- ingham offspring cohort [ J ]. Am J Respir Crit Care Med, 2009 (180) :3-10.
  • 7Diaz AA, Bartholmai B, San Jose Estepar R, et al. Relationship of emphysema and airway disease assessed by CT to exercise capacity in COPD [J]. RespirMed, 2010, 104(8) :1145-1151.
  • 8Fabbri LM, Luppi F, Beghe B, et al. Complex chronic comorbidi- ties of COPD [ J]. Eur Respir J, 2008, 31 ( 1 ) :204-212.
  • 9Wakayama K, Kurihara N, Fujimoto S, et al. Relationship between exercise capacity and the severity of emphysema as determined by high resolution CT[J]. Eur Resoir J. 1993.6(9) :1362-1367.
  • 10Bellomi M, Rampinelli C, Veronesi G, et al. Evolution of emphyse- ma in relation to smoking[J]. Eur Radiol, 2010, 20(2) : 286- 292.

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