Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-12-20
pubmed:abstractText
Based on our previous observations that 1-O-acetylbritannilactone (R)-4((3aS,4S,7aR)-4-hydroxy-6-methyl-3-methylene-2-oxo-2,3,3a,4,7,7a-hexahydrobenzofuran-5-yl)pentyl acetate (ABL) suppresses prostaglandin E(2) and nitric oxide synthesis in macrophages, the present study was designed to explore the effect of ABL on neointimal hyperplasia after balloon injury and its mechanism of action. In male Sprague-Dawley rats, 26 mg/kg ABL or polyglycol (control) was administered daily from 3 days before injury to 2 weeks after conventional balloon injury. ABL administration led to a significant reduction in neointimal formation (neointima to media ratio, 1.94 +/- 0.43 versus 0.84 +/- 0.29, P < 0.01) and proliferative activity of vascular smooth muscle cells after balloon injury in rats. Western blot analysis revealed that this is correlated to the inhibition of nuclear factor (NF)-kappaB activation and to the reduced expression of cyclooxygenase-2. Investigation of potential signaling pathways demonstrated that ABL inhibited NF-kappaB activation via the blockade of the inhibitor of NF-kappaB kinase-beta activation and the suppression of the degradation of the inhibitors of NF-kappaB-alpha. These findings suggest that ABL is a potential inhibitor of neointimal formation because it blocks injury-induced NF-kappaB activation and may have beneficial effects in reducing the risk of restenosis after angioplasty.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1521-0103
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
324
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
292-8
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Acetylbritannilactone Inhibits Neointimal Hyperplasia after Balloon Injury of Rat Artery by Suppressing Nuclear Factor-{kappa}B Activation.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, Institute of Basic Medicine, Hebei Medical University, No. 361, Zhongshan East Road, Shijiazhuang 050017, People's Republic of China. wjk@hebmu.edu.cn
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't