>
网站首页期刊介绍通知公告编 委 会投稿须知电子期刊广告合作联系我们
最新消息:
COPD大鼠气道上皮CC16 mRNA的表达及意义
作者:方苏榕  谷伟  谭焰  孙丽华 
单位:南京医科大学附属南京医院 呼吸内科,江苏 南京 210006
关键词:肺疾病 慢性阻塞性 克拉拉细胞分泌蛋白 噻托溴铵 炎症因子 大鼠 
分类号:R-33;R563
出版年·卷·期(页码):2014·33·第二期(162-167)
摘要:

目的:探讨CC16在慢性阻塞性肺病(COPD)发病机制中的作用。方法:将雄性SD大鼠随机分为健康对照组、COPD模型组(烟熏+内毒素)和噻托溴铵药物干预组,每组10只。RT-PCR检测各组大鼠气道上皮中CC16 mRNA的表达;免疫组化检测各组大鼠肺组织中CC16的蛋白表达;酶联免疫吸附试验(ELISA)检测各组大鼠血清中CC16、PLA2、IL8、TNFα的含量以及肺组织中PLA2、IL8、TNFα的含量。结果:大鼠气道上皮CC16 mRNA表达,COPD模型组较健康对照组显著减少,药物干预组较COPD模型组显著增加;血清及肺组织中CC16含量,COPD模型组较健康对照组显著减少,药物干预组较COPD模型组显著增加;血清及肺组织中PLA2、IL8、TNFα的含量,COPD模型组较健康对照组显著增多,药物干预组较COPD模型组显著减少(差异均有统计学意义,P<0.05)。结论:在COPD大鼠形成过程中,气道上皮CC16 mRNA表达及肺组织CC16蛋白表达显著减少,这一改变可能是其小气道损伤的组织学标志,且与COPD的发生与发展有关。

Objective: To explore the significance of CC16 in the pathogenesis of chronic obstructive pulmonary disease(COPD)by examining the CC16 expression in the airway epithelium of COPD rats before and after Tiotropium intervention. Methods: The male Sprague-Dawley(SD)rats were randomly assigned into the healthy control group, COPD model group(smoke+endotoxin), and Tiotropium intervention group, with 10 in each. RT-PCR was used to detect the gene expression of CC16 mRNA and immunohistochemistery was applied to test the protein expression of CC16 in the lung tissue in each group of rats. Enzyme-linked immunosorbent assay(ELISA)was adopted to investigate the levels of CC16, PLA2, IL8 and TNFα in the serum as well as PLA2, IL8, and TNFα in the lung tissue. Results: CC16 mRNA gene expression was significantly reduced in the lung tissue of COPD model group compared with the healthy control group, but remarkably increased in Tiotropium intervention group as opposed to COPD model group. CC16 was found to be higher in the serum and lung tissue of COPD model group and PLA2, IL8 and TNFα were lower than those in the healthy control group, while CC16 level was shown to be markedly elevated in the serum and lung tissue of Tiotropium intervention group and PLA2, IL8, and TNFα levels were significantly lower when compared with COPD model group. The differences were statistically significant(P<0.05). Conclusion: Gene expression of CC16 mRNA and CC16 protein expression in the airway epithelium decreased in the development of COPD rats, which may be a histological marker of mild airway injury in pathogenesis of COPD and involved in the development and progression of COPD.

参考文献:

[1] AGUSTI A,SOBRADILLO P,CELLI B.Addressing the complexity of chronic obstructive pulmonary disease:from phenotypes and biomarkers to scale-free networks,systems biology,and P4 medicine[J].Am J Respir Crit Care Med,2011,183(9):1129-1137.
[2] VALAVANIDIS A,VLACHOGIANNI T,FILTAKIS K.Tobacco smoke:involvement of reactive oxygen species and stable free radicals in mechanisms of oxidative damage,carcinogenesis and synergistic effects with other respirable particles[J].Int J Environ Res Public Health,2009,6(2):445-462.
[3] BROECKAERT F,BERNARD A.Clara cell secretory protein(CC16):characteristics and perspectives as lung peripheral biomarker[J].Clin Exp Allergy,2000,30(4):469-475.
[4] EMURA M.Stem cells of the respiratory tract[J].Paediatr Respir Rev,2002,3(1):36-40.
[5] MUTTI A,CORRADI M,GOLDONI M,et al.Exhaled metallic elements and serum pneumoproteins in asymptomatic smokers and patients with COPD or asthma[J].Chest,2006,129(5):1288-1297.
[6] BROECKAERT F,BERNARD A.Clara cell secretory protern(CC16):characteristics and perspectives as lung peripheral biomarker[J].Clin Exp Allergy,2000,30(4):469-475.
[7] 卞如镰,噻托溴铵治疗慢性阻塞性肺疾病独特的作用[J].国际呼吸杂志,2010,30(1):1-4.
[8] 邹春芳,谷伟,陈玉宝.沙美特罗替卡松联合呼吸操对慢性阻塞性肺疾病患者肺功能的影响[J].东南大学学报:医学版,2009,28(5):417-419.
[9] JEFFERY P K.Lymphocytes,chronic bronchitis and chronic obstructive pulmonary disease[J].Novartis Found Symp,2001,234:149-161;discussion 161-168.
[10] SPIRA A,BEANE J,SHAH V,et al.Effects of cigarette smoke on the human airway epithelial cell transcriptome[J].Proc Natl Acad Sci U S A,2004,101(27):10143-10148.
[11] TILLEY A E,O'CONNOR T P,HACKETT N R,et al.Biologic phenotyping of the human small airway epithelial response to cigarette smoking[J].PloS One,2011,6(7):e22798.
[12] INCORVAIA C,RIARIO-SFORZA G G,PRAVETTONI C,et al.Impairment of small airways in COPD patients with frequent exacerbations and effects of treatment with tiotropium[J].Int J Chron Obstruct Pulmon Dis,2008,3(1):123-126.
[13] 庞敏,王海龙,张彰,等.不同药物对COPD大鼠Clara细胞和CC16表达的影响[J].中国比较医学杂志,2008,18(2):1-4.
[14] De LUCA D,CAPOLUONGO E,RIGO V.Secretory phospholipase A2 pathway in various types of lung injury in neonates and infants:a multicentre translational study[J].BMC Pediatr,2011,11(8):101.
[15] FISHER C E,AHMAD S A,FITCH P M,et al.FITC-induced murine pulmonary inflammation:CC10 up-regulation and concurrent Shh expression[J].Cell Biol Int,2005,29(10):868-876.
[16] GOWDY K,KRANTZ Q T,DANIELS M,et al.Modulation of pulmonary inflammatory responses and antimicrobial defenses in mice exposed to diesel exhaust[J].Toxicol Appl Pharmacol,2008,229(3):310-319.

服务与反馈:
文章下载】【发表评论】【查看评论】【加入收藏
提示:您还未登录,请登录!点此登录
您是第 412838 位访问者


copyright ©《东南大学学报(医学版)》编辑部
联系电话:025-83272481 83272483
电子邮件:
bjb@pub.seu.edu.cn

苏ICP备09058364