摘要
为了探讨肺内调节肽在气道各类过敏性炎症发生、发展中的作用 ,我们观察了血管活性肠肽 (vasoactiveintestinalpeptide ,VIP)、表皮生长因子 (epidermalgrowthfactor,EGF)、内皮素 1(endothelin 1,ET 1)、降钙素基因相关肽(calcitoningene relatedpeptide ,CGRP)在未受应激与臭氧应激两种条件下对支气管上皮细胞 (bronchialepithelialcell,BEC)与嗜酸性粒细胞 (eosinophil,EOS)粘附的影响。结果发现 ,VIP、EGF可使O3应激的BEC与EOS的粘附率下降 ,下调气道上皮炎症反应 ;ET 1、CGRP可使未受应激的BEC与EOS的粘附率增加 ,诱发炎症损伤反应 ;CGRP还能加重臭氧的应激反应 ;ET 1、CGRP的效应可被W7、H7阻断。抗细胞间粘附分子 1(intercellularadhesionmolecule ,ICAM 1)抗体能阻断BEC与EOS的粘附 ,提示介导BEC与EOS粘附的粘附分子可能是ICAM 1。
To explore the roles of regulatory peptides in the process of various anaphylactic inflammation of the airway, we observed the influence of four peptides, i.e., vasoactive intestinal peptide (VIP), epidermal growth factor (EGF), endothelin 1 (ET 1), and calcitonin gene related peptide (CGRP), on the adhesion of eosinophil (EOS) to unstimulated and O 3 stressed bronchial epithlial cells (BEC). From the experiments we observed that VIP and EGF decreased EOS adherence to O 3 stressed BEC and downregulated airway inflammation; ET 1 and CGRP increased the adhesion of EOS to BEC in the inflammatory process; and CGRP aggravated O 3 stressed reactions.The effects of ET 1 and CGRP were inhibited by W 7 and H 7. Anti ICAM 1 antibody inhibited the adhesion of EOS to BEC, which brings to light that EOS adherence to BEC may be related to the expression of ICAM 1 of BEC.
出处
《生理学报》
CAS
CSCD
北大核心
2002年第1期43-46,共4页
Acta Physiologica Sinica
基金
ThisworkwassupportedbytheNationalNaturalScienceFoundationofChina (No 39770 635
3980 0 0 5 3)
