摘要
目的 探讨细胞间粘附分子 1(ICAM 1)在哮喘气道炎症粘附机制中的作用及糖皮质激素对哮喘大鼠血单个核细胞及肺组织ICAM 1表达的影响。方法 将SD大鼠随机分成哮喘组、地塞米松治疗组和正常对照组 ,采用免疫细胞化学和免疫组织化学研究各组大鼠血单个核细胞和肺组织ICAM 1表达情况。结果 (1)ICAM 1主要表达在肺小血管、毛细血管内皮细胞、支气管、肺泡上皮细胞、粘膜下基底膜及浸润的炎细胞上 ,哮喘组大鼠肺组织ICAM 1表达显著高于地塞米松治疗组和正常对照组 (P <0 0 5 )。 (2 )地塞米松组大鼠单个核细胞ICAM 1表达较哮喘组减轻 (P <0 0 5 )。 (3)治疗组大鼠肺组织和气管炎症反应以及气道反应性较哮喘组减轻。结论 证实了I CAM 1在哮喘炎性反应中的作用 ,地塞米松抑制ICAM 1表达。
Objective To investigate the adhesive mechanism of airway inflammation in the pathogenesis of asthma.Methods The SD rats were divided into asthma,dexamethasone and normal control groups at random.We studied the intercellular adhesion molecule-1(ICAM-1)on the peripheral blood mononuclear cells(PBMCs)and lung tissues of each rat by immunocytochemistry and immunohistochemisty.HE staining and electron microscope were used to define the inflammation in lung and trachea tissue.The largest tension of trachea to histamine was regarded as airway reactivity.Results (1)A significant increase in the ICAM-1 expression on the BMCos of asthmatic rats compared with those of the other groups.The distribution of ICAM-1 expression on the different part of lung tissue of asthmatic rats was similar to that of normal rats.ICAM-1 expression was rare on the endothelium of pulmonary artery and vein,on the bronchial and alveolar epithelium,and on the basal layer of the epithelium.But the level of ICAM-1 expression on the lung tissue of asthmatic rats was significantly increased compared with those of the other groups( P< 0.01).(2)Compared to asthmatic rats,lung inflammation and airway reactivity of the dexamethasone therapeutic groups was abated( P< 0.05).(3)The amount of total cells,eosinophil and lymphocyte in BALF of the dexamethasone therapeutic groups were significantly decreased compared to asthmatic rats( P< 0.01).Conclusions All the above suggests that ICAM-1 is involved in the inflammative adhesive mechanism of asthma and this provides a part of base for treating asthma with dexamethasone.
出处
《江苏医药》
CAS
CSCD
北大核心
2003年第7期499-502,共4页
Jiangsu Medical Journal