Quercetin inhibits inducible ICAM-1 expression in human endothelial cells through the JNK pathway
Quercetin inhibits inducible ICAM-1 expression in human endothelial cells through the JNK pathway
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DOI：
10.1152/ajpcell.1999.277.3.c403
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发表时间：
1999-09-01
影响因子：
5.5
通讯作者：
Packer, L
中科院分区：
文献类型：
--
作者：
Kobuchi, H;Roy, S;Packer, L
槲皮素通过JNK途径抑制人内皮细胞诱导的ICAM-1表达。点。[j] .中国生物医学工程学报，2009,31(2):387 - 398。细胞粘附分子细胞间粘附分子-1 （ICAM-1）在炎症反应中起关键作用。槲皮素（3,3',4',5,7-五羟基黄酮）是一种天然存在的膳食黄酮醇，具有有效的抗炎特性。研究槲皮素对激动剂phorbol 12-肉豆蔻酸13-乙酸酯（PMA）和肿瘤坏死因子- α (tnf - α)诱导的人内皮细胞ECV304 （ECV）中ICAM-1表达的影响。槲皮素处理以剂量依赖性（10-50 l-IM）的方式下调了ECV细胞中PMA-和tnf - α诱导的表面表达以及ICAM-1 mRNA水平。槲皮素对PMA-或tnf - α诱导的核因子- kb （NF-KB）活化无影响。然而，在类似的条件下，观察到激活蛋白1 （AP-1）激活的显著剂量依赖性下调。AP-1活化的降低与槲皮素对c-Jun nh2末端激酶（JNK）通路的抑制作用有关。这些结果表明槲皮素通过抑制AP-1激活和JNK途径下调PMA-和tnf - α诱导的ICAM-1表达。
Quercetin inhibits inducible ICAM-1 expression in human endothelial cells through the JNK pathway. Am. J. Physiol. 277 (Cell Physiol. 46): C403-C411, 1999.-The cell adhesion molecule intercellular adhesion molecule-1 (ICAM-1) plays a pivotal role in inflammatory responses. Quercetin (3,3',4',5,7-pentahydroxyflavone), a naturally occurring dietary flavonol, has potent anti-inflammatory properties. The effect of quercetin on ICAM-1 expression induced by agonists phorbol 12-myristate 13-acetate (PMA) and tumor necrosis factor-alpha (TNF-alpha) in human endothelial cell line ECV304 (ECV) was investigated. Quercetin treatment downregulated both PMA- and TNF-alpha-induced surface expression, as well as the ICAM-1 mRNA levels, in ECV cells in a dose-dependent (10-50 l-IM) manner. Quercetin had no effect on PMA- or TNF-alpha-induced nuclear factor-KB (NF-KB) activation. However, under similar conditions a remarkable dose-dependent downregulation of activator protein-1 (AP-1) activation was observed. This decrease in AP-1 activation was observed to be associated with the inhibitory effects of quercetin on the c-Jun NH2-terminal kinase (JNK) pathway. These results suggest that quercetin downregulates both PMA- and TNF-alpha-induced ICAM-1 expression via inhibiting both AP-1 activation and the JNK pathway.