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1‐Furan‐2‐yl‐3‐Pyridin‐2‐yl‐Propenone inhibits TNF‐¥á‐induced intestinal inflammation via suppression of MCP‐1 and IL‐8 expressions in HT‐29 human colon epithelial cells
Author(s) -
Kim KyoungJin,
Park SuYoung,
Lee Jong Suk,
Lee Eung Seok,
Kim JungAe
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.649
Subject(s) - inflammation , inflammatory bowel disease , chemistry , pharmacology , tumor necrosis factor alpha , proinflammatory cytokine , colitis , in vitro , interleukin 8 , interleukin , immunology , cytokine , medicine , biochemistry , disease
Previously, we have shown that 1‐Furan‐2‐yl‐3‐Pyridin‐2‐yl‐Propenone (FPP‐3) has an anti‐inflammatory and anti‐invasive activity. In the present study, we investigated an inhibitory effect of FPP‐3 on the TNF‐α‐induced inflammatory response in HT‐29 human colon epithelial cells in vitro. Treatment with FPP‐3 significantly prevented the attachment of leukocytes to HT29 colon epithelial cells, one of the pathologic hallmarks in colon inflammation. The effect of FPP‐3 was comparable to that of 5‐aminosalicylic acid, a commonly used drug in the treatment of inflammatory bowel disease (IBD). In addition, FPP‐3 significantly suppressed NF‐κB transcription activity. The pretreatment with FPP‐3 inhibited TNF‐α‐induced MCP‐1 interleukin‐8 mRNA expressions. These results demonstrate that FPP‐3 modulates intestinal inflammation via suppressing the expression of inflammatory cytokines, and suggest that FPP‐3 may be a valuable agent for the treatment of IBD.