摘要
目的探讨纤维蛋白溶解酶原激活物抑制剂（PAI）－1、组织型纤维蛋白溶解酶原激活物（t—PA）、尿激酶型纤维蛋白溶解酶原激活物（u－PA）及其受体（u－PAR）在支气管哮喘（简称哮喘）患者诱导痰中的表达及意义。方法用ELISA法分别检测29例哮喘急性发作者（发作组）、26例缓解者（缓解组）及15例健康对照者（对照组）诱导痰中PAI－1、t-PA、u—PA和u－PAR的含量，同期测定肺功能（第1秒用力呼气容积占预计值百分比，FEV，％pred），并进行比较。结果发作组和缓解组诱导痰PAI－1、u—PAR含量[分别为（23．32±2t．64）、（0．766±0．272）μg／L和（17．23±9．40）、（0．700±0．271）μg／L]较对照组[（5．99±5．04）、（O．516±0．197）μg／L3均明显升高（P〈0．05）。而三组诱导痰u—PA、t-PA含量[分别为（O．287±0．235）、（7．68±3．46）μg／L，（0．251±0．276）、（9．88±4．68）μg／L，（0．239±0．322）、（10．35±7．47）μg／L]比较差异均无统计学意义（P〉0．05）。缓解组诱导痰PAI-1与FEV1 % pred呈负相关（r=-0．756，P〈0．01）。缓解组诱导痰PAI-1与病程呈正相关（r=0．454，P〈0．05）。结论PAI-1、u-PAR参与了哮喘气道慢性炎性反应的病理生理过程。
Objective To detect the levels of plasminogen activator inhibitor （PAI）-1,tissue plas- minogen activator（t-PA ）, urokinase-type plasminogen activator（u-PA） and urokinase-type plasminogen activator receptor （u-PAR） in induced sputum in patients with asthma and analyze their clinical significanees in pathogenesis of asthma. Methods The induced sputum was isolated from 15 normal subjects （control group ）, 29 patients with acute attack of asthma （attack group） and 26 stable asthma patients （ stable group）. The levels of PAI-1, t-PA, u-PA and u-PAR were measured by ELISA. Meanwhile FEV1%pred of all groups were evaluated. Results The levels of PAI-1 and u-PAR of induced sputum were significantly higher in attack group [ （23.32±21.64）, （0.766 ± 0.272） μg/L ] and stable group [ （ 17.23 ± 9.40）, （0.700 ± 0.271 ）μg/L ] than those in control group [ （ 5.99 ± 5.04）, （0.516 ±0.197 ）μg/L ] （P 〈 0.05 ）. As for the induced sputum concentrations of u-PA and t-PA, there were no significant differences among the attack group [（0.287 ± 0.235）,（7.68 ± 3.46） μg/L], stable group [（0.251 ± 0.276）,（9.88 ±4.68）μg/L] and control group [ （0.239 ± 0.322）,（ 10.35± 7.47 ） μg/L]. In stable group, the level of PAI-1 had a negative correlation with the FEVl%pred （r = -0.756, P 〈 0.01 ）. In stable group, the level of PAI-1 had a positive correlation with the length of disease course （r=- 0.454, P 〈 0.05）. Conclusion PAl-1 and u-PAR maybe involved in pathophysiologic change of asthma.
出处
《中国医师进修杂志（内科版）》
2009年第1期1-3,共3页
Chinese Journal of Postgraduates of Medicine
