期刊
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
卷 324, 期 1, 页码 292-298出版社
AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
DOI: 10.1124/jpet.107.127407
关键词
-
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)-kappa B activation and to the reduced expression of cyclooxygenase-2. Investigation of potential signaling pathways demonstrated that ABL inhibited NF-kappa B activation via the blockade of the inhibitor of NF-kappa B kinase-beta activation and the suppression of the degradation of the inhibitors of NF-kappa B-alpha. These findings suggest that ABL is a potential inhibitor of neointimal formation because it blocks injury-induced NF-kappa B activation and may have beneficial effects in reducing the risk of restenosis after angioplasty.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据