Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.10 (IKK)
 4,900 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Acetylbritannilactone Inhibits Neointimal Hyperplasia after Balloon Injury of Rat Artery by Suppressing Nuclear Factor-{kappa}B Activation. 1791 74