《中国康复理论与实践》 ›› 2006, Vol. 12 ›› Issue (01): 41-42.

• 基础研究 • 上一篇    下一篇

糖皮质激素对哮喘大鼠气道上皮细胞NF-κB、ICAM-1表达的影响

王宏伟; 邵玉霞; 梁蕊   

  1. 哈尔滨医科大学附属第二医院呼吸科 黑龙江哈尔滨市 150086
  • 收稿日期:2005-11-01 出版日期:2006-01-25 发布日期:2006-01-25

Effects of inhaled budesonide on the expression of nuclear factor-κB and intercellular adhesion molecule-1 in airway epithelial cells of asthma rats

WANG Hong-wei, SHAO Yu-xia, LIANG Rui   

  1. Department of Respiration, Affiliated 2nd Hospital, Harbin Medical University, Harbin 150086, Heilongjiang, China
  • Received:2005-11-01 Published:2006-01-25 Online:2006-01-25

摘要: 目的探讨糖皮质激素(布地奈德混悬液)对核因子-κB(NF-κB)、细胞间粘附分子-1(ICAM-1)在哮喘大鼠气道上皮细胞表达的影响。方法将30只大鼠随机分为对照组、哮喘组、布地奈德治疗组,应用免疫组化技术结合计算机病理图像分析系统测定大鼠气道上皮胶原的沉积和气道上皮细胞NF-κB、ICAM-1的相对含量。结果哮喘组NF-κB、ICAM-1的表达水平、气道上皮胶原的沉积明显高于对照组及布地奈德治疗组(均P<0.01),气道上皮细胞NF-κB与ICAM-1表达呈正相关(r=0.61,P<0.01),ICAM的表达水平与气道上皮胶原含量呈正相关(r=0.47,P<0.01)。结论NK-κB、ICMA-1在哮喘气道重构的发生机制中发挥重要作用,早期应用布地奈德可能通过下调NF-κB、ICAM-1的表达,干预气道重构。

关键词: 哮喘, 气道重构, 核因子-κB(NF-κB), 细胞间粘附分子-1(ICAM-1), 糖皮质激素

Abstract: ObjectiveTo investigate the effects of early inhaled budesonide on the expression of nuclear factor-kappa B(NF-κB) and intercellular adhesion molecule(ICAM-1) in airway epithelial cells of asthma rats.Methods30 rats were randomly divided into three groups:control group, asthma group and therapeutic group with inhaled budesonide.The expression of NF-κB and ICAM-1 in bronchial epithelium were observed with immunohistochemical staining and computer image analysis system.ResultsThe expression of NF-κB, ICAM-1 and subepithelial collagen deposition were significantly highly in asthma group than those of control group and of therapeutic group (P<0.01 respectively). There was a close correlation between the expression of NF-κB and ICAM-1 in asthma rats (r=0.61,P<0.01), as well as between the expression of ICAM-1 and supepithelial collagen(r=0.47,P<0.01).ConclusionThe excessive expression of NF-κB and ICAM-1 play an important role in the pathogenesis of airway remodeling in asthma.Budesonide can influence airway remodeling by downregulating the expression of NF-κB and ICAM-1.

Key words: asthma, airway remodeling, nuclear factor-kappa B(NF-κB), intercellular adhesion molecule(ICAM-1), glucocorticoid