论文部分内容阅读
目的:评价细胞间粘附分子1(ICAM-1)、P选择素在哮喘气道炎症粘附机制中的作用,进一步阐明哮喘的发病机理。方法:用酶联免疫吸附试验、肺组织免疫组化检查和呼吸生理学方法系统观察正常组和哮喘组豚鼠各项指标。结果:(1)哮喘组豚鼠肺潮气量、动态肺顺应性(Cdyn)和肺气道阻力与对照组比较差异有显著性(P<0.01及P<0.05)。(2)哮喘组豚鼠血浆和肺泡灌洗液(BALF)可溶性ICAM-1(sICAM-1)、可溶性P选择素、血清和BALF嗜酸粒细胞阳离子蛋白(ECP)与对照组比较,差异有显著性(P<0.01);BALF中白细胞介素8(IL-8)与对照组比较差异也有显著性(P<0.01)。(3)哮喘组豚鼠肺组织(气道上皮和血管内皮)ICAM-1和IL-8表达与对照组比较,差异有显著性(P<0.01)。结论:ICAM-1、P选择素、IL-8、ECP参与介导了哮喘气道炎症的粘附过程。
OBJECTIVE: To evaluate the role of ICAM-1 and P-selectin in the airway inflammation and adhesion mechanisms in asthma and further elucidate the pathogenesis of asthma. Methods: The indexes of guinea pigs in normal group and asthma group were observed by enzyme-linked immunosorbent assay, immunohistochemistry of lung tissue and respiratory physiology. Results: (1) The lung tidal volume, dynamic lung compliance (Cdyn) and pulmonary airway resistance in asthma group were significantly different from those in control group (P <0.01 and P <0.05). (2) Compared with control group, soluble ICAM-1, soluble P-selectin, serum and BALF eosinophil cationic protein (ECP) in plasma and BALF of asthmatic guinea pigs were significantly different (P <0.01). IL-8 in BALF was also significantly different from that in control group (P <0.01). (3) Compared with control group, the expression of ICAM-1 and IL-8 in lung tissue (airway epithelium and vascular endothelium) in asthmatic group were significantly different (P <0.01). Conclusion: ICAM-1, P-selectin, IL-8 and ECP are involved in the process of airway inflammation in asthma.