Inhibitory effect of luteolin on TNF-α-induced IL-8 production in human colon epithelial cells
Inhibitory effect of luteolin on TNF-α-induced IL-8 production in human colon epithelial cells
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DOI：
10.1016/j.intimp.2004.09.027
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发表时间：
2005-01-01
影响因子：
5.6
通讯作者：
Lee, YM
中科院分区：
文献类型：
--
作者：
Kim, JA;Kim, DK;Lee, YM
白细胞介素（IL）-8在炎症性肠病中的炎症反应的启动和维持中起核心作用。IL-8的促炎性产生需要多种激酶的活化，这导致IkappaB降解和NF-κ B活化。在这项研究中，我们研究了木樨草素，一种主要的黄酮类化合物，对TNF-α诱导的人结肠上皮细胞IL-8的产生的作用。在存在或不存在毛地黄黄酮的情况下，用TNF-α刺激HT 29细胞。酶联免疫吸附试验（ELISA）和逆转录聚合酶链反应（RT-PCR）检测IL-8的产生，Western blot检测丝裂原活化蛋白激酶（MAPKs）的活化和IkappaB的降解。NF-κ B活化通过电泳运动位移测定（EMSA）评估。木犀草素以剂量依赖性方式抑制TNF-α诱导的IL-8产生。此外，木樨草素抑制TNF-α诱导的p38 MAPK和细胞外调节激酶（ERK）磷酸化、IkappaB降解和NF-κ B活化。这些结果表明，毛地黄黄酮通过阻断MAPK的磷酸化而对TNT-α诱导的肠上皮细胞中IL-8的产生具有抑制作用。随后IkappaB降解和NF-κ B活化。(C)2004 Elsevier B. V.保留所有权利。
Interleukin (IL)-8 plays a central role in the initiation and maintenance of inflammatory responses in the inflammatory bowel disease. The proinflammatory cytokine-mediated production of IL-8 requires activation of various kinases, which leads to the IkappaB degradation and NF-kappaB activation. In this study, we investigated the role of luteolin, a major flavonoid of Lonicera japonica, on TNF-alpha-induced IL-8 production in human colonic epithelial cells. HT29 cells were stimulated with TNF-alpha in the presence or absence of luteolin. IL-8 production was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis, and the mitogen-activated protein kinases (MAPKs) activation and IkappaB degradation were determined by Western blot analysis. NF-kappaB activation was assessed by the electrophoretic motility shift assay (EMSA). Luteolin suppressed TNF-alpha-induced IL-8 production in dose-dependent manner. In addition, luteolin inhibited TNF-alpha-induced phosphorylation of p38 MAPK and extracellular-regulated kinases (ERK), IkappaB degradation, and NF-kappaB activation. These results suggest that luteolin has the inhibitory effects on TNT-alpha-induced IL-8 production in the intestinal epithelial cells through blockade in the phosphorylation of MAPKs. following IkappaB degradation and NF-kappaB activation. (C) 2004 Elsevier B.V. All rights reserved.