Source:http://linkedlifedata.com/resource/pubmed/id/15472516
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
|
| pubmed:dateCreated |
2004-10-8
|
| pubmed:abstractText |
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-alpha (TNF-alpha)-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-alpha-mediated p38 and extracellular signal-regulated kinase (ERK) phosphorylation. Further, CATP reduced NF-kappaB-mediated transcriptional activation as well as Ikappa-Balpha 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-alpha, interleukin-1beta, and intercellular adhesion molecule-1 along with the inhibition of NF-kappa 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.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Sep
|
| pubmed:issn |
1078-0998
|
| pubmed:author |
pubmed-author:ChoiEun-YoungEY,
pubmed-author:ChoiSuck-CheiSC,
pubmed-author:ChungHun-TaegHT,
pubmed-author:JunChang-DukCD,
pubmed-author:KimKyoung-SukKS,
pubmed-author:KimSang-WookSW,
pubmed-author:KimSoonhagS,
pubmed-author:KimTae-HyeonTH,
pubmed-author:KimYoun-SeokYS,
pubmed-author:KimmKu-ChanKC,
pubmed-author:LeeHyun-JuHJ,
pubmed-author:LeeMoo-HyungMH,
pubmed-author:OhBerm-SeokBS,
pubmed-author:OhHyun-CheolHC,
pubmed-author:OhHyun-MeeHM,
pubmed-author:OhJae-MinJM,
pubmed-author:PaeHyun-OckHO,
pubmed-author:ParkDo-SimDS,
pubmed-author:SeoGeom-SeogGS,
pubmed-author:WooWon-HongWH
|
| pubmed:copyrightInfo |
Copyright 2004 Lippincott Williams & Wilkins
|
| pubmed:issnType |
Print
|
| pubmed:volume |
10
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
564-72
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:15472516-Animals,
pubmed-meshheading:15472516-Colitis,
pubmed-meshheading:15472516-Cytokines,
pubmed-meshheading:15472516-Disease Models, Animal,
pubmed-meshheading:15472516-Down-Regulation,
pubmed-meshheading:15472516-Gene Expression Regulation,
pubmed-meshheading:15472516-Glucosides,
pubmed-meshheading:15472516-Inflammation,
pubmed-meshheading:15472516-Intestinal Mucosa,
pubmed-meshheading:15472516-Male,
pubmed-meshheading:15472516-Mice,
pubmed-meshheading:15472516-Mice, Inbred BALB C,
pubmed-meshheading:15472516-Severity of Illness Index,
pubmed-meshheading:15472516-Signal Transduction,
pubmed-meshheading:15472516-Trinitrobenzenes
|
| pubmed:year |
2004
|
| pubmed:articleTitle |
Catalposide, 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.
|
| pubmed:affiliation |
Digestive Disease Research Institute, Department of Microbiology and Immunology, Wonkwang University School of Medicine, Iksan, Chonbuk 570-749, Seoul 122-701, Korea.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|