Inhibitory effect of luteolin on TNF-α-induced IL-8 production in human colon epithelial cells

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 IκB degradation and NF-κB activation. In this stu...

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Published inInternational immunopharmacology Vol. 5; no. 1; pp. 209 - 217
Main Authors Kim, Jin-A, Kim, Dae-Ki, Kang, Ok-Hwa, Choi, Yeon-A, Park, Hye-Jung, Choi, Suck-Chei, Kim, Tae-Hyun, Yun, Ki-Jung, Nah, Yong-Ho, Lee, Young-Mi
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier B.V 2005
Elsevier
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Summary: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 IκB degradation and NF-κB activation. In this study, we investigated the role of luteolin, a major flavonoid of Lonicera japonica, on TNF-α-induced IL-8 production in human colonic epithelial cells. HT29 cells were stimulated with TNF-α 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 IκB degradation were determined by Western blot analysis. NF-κB activation was assessed by the electrophoretic motility shift assay (EMSA). Luteolin suppressed TNF-α-induced IL-8 production in dose-dependent manner. In addition, luteolin inhibited TNF-α-induced phosphorylation of p38 MAPK and extracellular-regulated kinases (ERK), IκB degradation, and NF-κB activation. These results suggest that luteolin has the inhibitory effects on TNF-α-induced IL-8 production in the intestinal epithelial cells through blockade in the phosphorylation of MAPKs, following IκB degradation and NF-κB activation.
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ISSN:1567-5769
1878-1705
DOI:10.1016/j.intimp.2004.09.027