Linked Life Data

18549679

Source:http://linkedlifedata.com/resource/pubmed/id/18549679

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2008-6-13
pubmed:abstractText
Eutigoside C, a compound isolated from the leaves of Eurya emarginata, is thought to be an active anti-inflammatory compound which operates through an unknown mechanism. In the present study we investigated the molecular mechanisms of eutigoside C activity in lipopolysacchardide (LPS)-stimulated murine macrophage RAW 264.7 cells. Treatment with eutigoside C inhibited LPS-stimulated production of nitric oxide (NO), prostaglandin E(2) (PGE(2)) and interleukin-6 (IL-6). To further elucidate the mechanism of this inhibitory effect of eutigoside C, we studied LPS-induced nuclear factor (NF)-kappaB activation and mitogen-activated protein (MAP) kinase phosphorylation. Eutigoside C suppressed NF-kappaB DNA binding activity, interfering with nuclear translocation of NF-kappaB. Eutigoside C suppressed the phosphorylation of three MAP kinases (ERK1/2, JNK and p38). These results suggest that eutigoside C inhibits the production of inflammatory mediators (NO, PGE(2) and interleukin-6) by suppressing the activation and translocation of NF-kappaB and the phosphorylation of MAP kinases (ERK1/2, JNK and p38) in LPS-stimulated murine macrophage RAW 264.7 cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-3573
pubmed:author
pubmed:issnType
Print
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
917-24
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Eutigoside C inhibits the production of inflammatory mediators (NO, PGE(2), IL-6) by down-regulating NF-kappaB and MAP kinase activity in LPS-stimulated RAW 264.7 cells.
pubmed:affiliation
Department of Pharmacology, College of Medicine, Cheju National University, Jeju 690-756, South Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't