Open AccessCatalposide, a compound isolated from Catalpa Ovata , attenuates induction of intestinal epithelial proinflammatory gene expression and reduces the severity of trinitrobenzene sulfonic acid‐induced colitis in mice
Author(s) -
Kim SangWook,
Choi SuckChei,
Choi EunYoung,
Kim KyoungSuk,
Oh JaeMin,
Lee HyunJu,
Oh HyunMee,
Kim Soonhag,
Oh BermSeok,
Kimm KuChan,
Lee MooHyung,
Seo GeomSeog,
Kim TaeHyeon,
Oh HyunCheol,
Woo WonHong,
Kim YounSeok,
Pae HyunOck,
Park DoSim,
Chung HunTaeg,
Jun ChangDuk
Publication year - 2004
Publication title -
inflammatory bowel diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.932
H-Index - 146
eISSN - 1536-4844
pISSN - 1078-0998
DOI - 10.1097/00054725-200409000-00010
Subject(s) - proinflammatory cytokine , colitis , tumor necrosis factor alpha , signal transduction , pharmacology , in vivo , inflammation , medicine , chemistry , immunology , biology , biochemistry , microbiology and biotechnology
Certain irinoid‐producing plants have been used as herbal anti‐inflammatory remedies. Here we evaluated whether catalposide (CATP), a single compound isolated from irinoid‐producing plant Catalpa ovata , has a potential for preventing or ameliorating diseases characterized by mucosal inflammation. Preliminary microarray‐based gene expression test revealed that CATP, which alone did not significantly affect expression of any of the >8,000 genes analyzed, attenuated the expression of tumor necrosis factor‐α (TNF‐α)‐induced proinflammatory genes including interleukin‐8 (IL‐8) in human intestinal epithelial HT‐29 cells. Down‐regulation of IL‐8 mRNA accumulation was also reflected by the decreased IL‐8 secretion in CATP‐treated HT‐29 cells. The signal transduction study revealed that CATP significantly attenuates TNF‐α‐mediated p38 and extracellular signal‐regulated kinase (ERK) phosphorylation. Further, CATP reduced NF‐κB‐mediated transcriptional activation as well as Iκ‐Bα degradation. To establish the in vivo relevance of these findings, we examined whether CATP could affect intestinal inflammation in vivo using the mouse model of trinitrobenzene sulfonic acid (TNBS)‐induced inflammatory colitis. Intrarectal administration of CATP dramatically reduced the weight loss, colonic damage, and mucosal ulceration that characterize TNBS colitis. Moreover, CATP suppressed the expression of TNF‐α, interleukin‐1β, and intercellular adhesion molecule‐1 along with the inhibition of NF‐κ B p65 translocation into nucleus in TNBS colitis. Collectively, current results demonstrate that CATP may be an effective agent for the treatment of diseases characterized by mucosal inflammation.