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肺内调节肽对支气管上皮细胞ICANF 1表达及NF- #Kappa#B活性的调控

谭宇蓉, 秦晓群, 管茶香, 张长青, 罗自强, 孙秀泓

中南大学湘雅医学院牛理学教研室.长沙410078

摘要

细胞间粘附分子一1 (ICAM-1)是介导细胞与细胞之间粘附的重要生物分子;核因子一KB ( NF-KB)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-KB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-KB活性的影响，以及NF-KB抑制剂MG132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-KB制剂MG132可阻断q.ET-1 .CGRP引起的ICAM-1表达，提示NF-KB在调控ICAM-1表达中起重要作用。E M-A结果显示，BECs中NF-KB在臭氧应激下反复激活，CGRP与ET1可促进NF- KB的激活;VIP与E GF可抑制臭氧应激的BECs中NF-KB的激活。以上结果说明，VIP .EGF可通过下调ICAM-1转录及NF-KB激活减轻炎症反应，而ET-1 .CGRP可通过上调ICAM-1转录及NF-KB激活、加大炎症反应。ICAM-1与NF- KB的持续表达和反复激活是炎症持续加重发展的重要因素。

关键词： 肺内调节肽; 细胞间粘附分子一1; 核因子一KB; 支气管上皮细胞

Regulatory peptides modulate I CAM 1 gene expression and NF #kappa#B activity in bronchial epithelial cells

TAN Yu Rong, QIN Mao- Qun, GUAN Cha Xiang, ZHANG Chang Qing, LUO Zi Qiang, SUN Xiu Hong

Department of Physiology，Xiangya School of Medicine，Central South University，Changsha 410078

Abstract

Intercellular adhesion molecule-1(ICAM-1)is an important adhesion molecule leading to adhesion between cells;NFKB，being universally distributed in the organism，is an important nuclear transcription factor leading to a rapid response to the stimuli .Line of evidence have shown that ICAM-1 transcription and NF-KB activation is an important step of inflammatory reaction.To test that intrapulmonary regulatory peptides modulate inflammatory lesion of bronchial epithelial cells(BECs) through their effect on ICAM-1 expression and nuclear factor KB(NF- KB) activation，we used immunocytochemistry，RT PCR, and electrophoretic mobility- shift assay(EMSA) to determine the ICAM-1 expression and NF-KB activity in BECs.The effects of NF-KB inhibitor MG 132 on ICA1vF1 expression were also observed.The results showed that vasoactive intestinal peptide(VIP) and epidermal growth
factor(EGF) decreased ICAM-1 expression in O3-stressed BECs，while endothelirrl(ET-1)and calcitonin gene related peptides (CGRP) increased ICAIYFI expression in resting BECs.MG132 blocked ICA1vF1 expression induced byq，ET-1 and CGRP.
The results obtained by using EMSA confirmed that VIP and EGF restrained the activation of NF-KB inq一stressed BECs;CGRP and ET -1 promoted activation of NF-KB.These observations indicate that VIP and EGF abated the injury by means of dowrr regulatory effects on ICAM-1 transcription and NF-#Kappa#B activation，while ET -1 and CGRP enhanced the inflammation reaction by an up regulatory effect .It is suggested that a developing and intensive airway inflammation correlates closely with a persistent expression of ICAIYFI and repeated activation of NF- #Kappa#B.

Key words: intrapulmonary regulatory peptides;intercellular adhesion molecule-1(ICAM-1);nuclear factor KB(NF-KB);hrnnchial Pithpfal PPllc

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引用本文：

谭宇蓉, 秦晓群, 管茶香, 张长青, 罗自强, 孙秀泓. 肺内调节肽对支气管上皮细胞ICANF 1表达及NF- #Kappa#B活性的调控[J]. 生理学报 2003; 55 (2): .

TAN Yu Rong, QIN Mao- Qun, GUAN Cha Xiang, ZHANG Chang Qing, LUO Zi Qiang, SUN Xiu Hong. Regulatory peptides modulate I CAM 1 gene expression and NF #kappa#B activity in bronchial epithelial cells. Acta Physiol Sin 2003; 55 (2): (in Chinese with English abstract).