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细胞间粘附分子 1(ICAM 1)是介导细胞与细胞之间粘附的重要生物分子 ;核因子 κB (NF κB)是体内普遍存在、能迅速对刺激产生反应的重要核转录因子。越来越多的证据显示 ,ICAM 1表达与NF κB激活是炎症反应的重要步骤。我们应用免疫组化、RT PCR、凝胶阻滞电泳 (EMSA)等多种实验方法 ,观察了肺内调节肽对支气管上皮细胞ICAM 1表达及NF κB活性的影响 ,以及NF κB抑制剂MG 13 2对ICAM 1表达的影响。实验结果发现 ,VIP、EGF可使臭氧应激BECs的ICAM 1表达降低 ;ET 1、CGRP可使未受应激BECs的ICAM 1表达增加。NF κB抑制剂MG 13 2可阻断O3、ET 1、CGRP引起的ICAM 1表达 ,提示NF κB在调控ICAM 1表达中起重要作用。EM SA结果显示 ,BECs中NF κB在臭氧应激下反复激活 ,CGRP与ET 1可促进NF κB的激活 ;VIP与EGF可抑制臭氧应激的BECs中NF κB的激活。以上结果说明 ,VIP、EGF可通过下调ICAM 1转录及NF κB激活减轻炎症反应 ,而ET 1、CGRP可通过上调ICAM 1转录及NF κB激活、加大炎症反应。ICAM 1与NF κB的持续表达和反复激活是炎症持续加重发展的重要因素
Intercellular adhesion molecule 1 (ICAM 1) is an important biological molecule that mediates adhesion between cells and cells. Nuclear factor κB (NF κB) is an ubiquitous nuclear transcription factor that can rapidly respond to stimuli in vivo. There is growing evidence that ICAM 1 expression and NF κB activation are important steps in the inflammatory response. We used immunohistochemistry, RT PCR, gel electrophoresis (EMSA) and other experimental methods to observe the effects of pulmonary regulatory peptides on the expression of ICAM 1 and the activity of NF κB in bronchial epithelial cells, as well as the effects of NF κB inhibitor MG 13 2 on ICAM 1 expression. The experimental results showed that VIP and EGF can reduce the expression of ICAM 1 in ozone-stressed BECs, and ET 1 and CGRP can increase the expression of ICAM-1 in unstressed BECs. NF-κB inhibitor MG13 2 blocked ICAM-1 expression induced by O3, ET1 and CGRP, suggesting that NF-κB plays an important role in the regulation of ICAM-1 expression. EM SA results showed that NFκB in BECs was activated repeatedly under ozone stress. CGRP and ET 1 promoted the activation of NFκB; VIP and EGF inhibited NFκB activation in ozone-stressed BECs. The above results show that VIP and EGF can reduce the inflammatory response by down-regulating the transcription of ICAM-1 and the activation of NF-κB, while ET 1 and CGRP can increase the inflammatory reaction by up-regulating ICAM-1 transcription and NF-κB activation. Sustained expression and reactivation of ICAM 1 and NF κB are important factors in the persistent worsening of inflammation