The role of cell adhesion molecules in airway inflammation in a rat model of chronic obstructive pulmonary disease

ZHEN Chunfang; et al

doi:10.13406/j.cnki.cyxb.2004.05.025

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The role of cell adhesion molecules in airway inflammation in a rat model of chronic obstructive pulmonary disease

更新时间：2024-01-17

- The role of cell adhesion molecules in airway inflammation in a rat model of chronic obstructive pulmonary disease
- Journal of Chongqing Medical University Issue 5, Pages: 644-647(2004)
- 作者机构：
  
  1. 重庆医科大学临床学院肺科
  2. 重庆医科大学临床学院肺科,重庆,400016
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.2004.05.025
  CLC： R563.9
- Published：2004，
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[1]曾春芳,吴亚梅.细胞粘附分子在慢性阻塞性肺疾病大鼠气道炎症中的作用[J].重庆医科大学学报,2004(05):644-647+681.

ZHEN Chunfang, et al. The role of cell adhesion molecules in airway inflammation in a rat model of chronic obstructive pulmonary disease. [J]. Journal of Chongqing Medical University (5):644-647(2004)
[1]曾春芳,吴亚梅.细胞粘附分子在慢性阻塞性肺疾病大鼠气道炎症中的作用[J].重庆医科大学学报,2004(05):644-647+681. DOI： 10.13406/j.cnki.cyxb.2004.05.025.

ZHEN Chunfang, et al. The role of cell adhesion molecules in airway inflammation in a rat model of chronic obstructive pulmonary disease. [J]. Journal of Chongqing Medical University (5):644-647(2004) DOI： 10.13406/j.cnki.cyxb.2004.05.025.

摘要

目的 :制备慢性阻塞性肺疾病（COPD）大鼠模型

探讨细胞间粘附分子 - 1（ICAM - 1）、E -选择素在COPD气道炎症中的作用。方法 :Wistar大鼠 2 0只随机分为对照阻（A组

10只）、模型组（B组

10只） ;采用两次气管内注入脂多糖（LPS）和反复烟熏的方法制作COPD大鼠模型 ;采用免疫组化法检测ICAM - 1、E -选择素在COPD大鼠支气管肺组织中的表达。结果 :所建大鼠模型的病理及病理生理学改变基本符合人类COPD的特点 ;模型组支气管上皮细胞、肺泡上皮细胞及支气管肺组织微小血管内皮细胞ICAM - 1表达强度显著高于对照组（P <0 .0 1）

且与支气管肺泡灌洗夜（BALF）中白细胞总数及中性粒细胞数成显著正相关（分别为 :r =0 .76

P <0 .0 1;r =0 .6 5

P <0 .0 5 ） ;模型组支气管肺组织微小血管内皮细胞E -选择素的表达强度显著高于对照组（P <0 .0 1）

且与BALF白细胞总数及中性粒细胞数成显著正相关（分别为 :r =0 .82

P <0 .0 0 1;r =0 .79

P <0 .0 0 1）。结论 :ICAM - 1、E -选择素可能参与了COPD气道炎症过程。

Abstract

Objective:To study the role of intercellular adhesion molecule-1(ICAM-1) and E-selectin in the airway inflammation in a rat model of chronic obstructive pulmonary disease(COPD).Methods:20 Wistar rats were randomly divided into two groups:the control group(group A

10 rats) and the model group (group B

10 rats).COPD rat model was established by intratracheal instillation of lipopolysacharide(LPS) twice and exposure to cigarette smoke daily;the expression of ICAM-1 and E-selectin in rat lung tissue was detected by means of immunohistochemistry(sp).Results:The changes in histopathology and pathophysiology in the animal model were similar to those in COPD patients.The expression of ICAM-1 on bronchi and alveolar epithelial and bronchopulmonary capillary endothelial cells of the model significantly increased as compared with the control group( P <0.01) and was positively correlated with the leukocyte numbers and neutrophils in BALF in the model group( r=0.76

P<0.01;r=0.65

P<0.05

respectively).The expression of E-selectin on bronchopulmonary capillary endothelial cells the of the model group significantly increased as compared with the control group ( P <0.01)and was positively correlated with the leukocyte numbers and neutrophils in BALF in the model group (r=0.82

P<0.001;r=0.79

P<0 .001

respectively).Conclusion:ICAM-1 and E-selectin may be involved in the process of airway inflammation in COPD.

关键词

细胞间粘附分子-1选择素炎症慢性阻塞性肺疾病

Keywords

ICAM-1E-selectininflammationCOPD

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