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

• Published in: International immunopharmacology 2005-01, Vol.5 (1), p.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: Article
• Language: English
• Subjects: Lonicera japonica
• ISSN: 1567-5769
• DOI: 10.1016/j.intimp.2004.09.027

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 I mu B degradation and NF- mu B activation. In this study, we investigated the role of luteolin, a major flavonoid of Lonicera japonica, on TNF-induced IL-8 production in human colonic epithelial cells. HT29 cells were stimulated with TNF- 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 I mu B degradation were determined by Western blot analysis. NF- mu B activation was assessed by the electrophoretic motility shift assay (EMSA). Luteolin suppressed TNF-induced IL-8 production in dose-dependent manner. In addition, luteolin inhibited TNF-induced phosphorylation of p38 MAPK and extracellular-regulated kinases (ERK), I mu B degradation, and NF- mu B activation. These results suggest that luteolin has the inhibitory effects on TNF-induced IL-8 production in the intestinal epithelial cells through blockade in the phosphorylation of MAPKs, following I mu B degradation and NF- mu B activation.