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Polyaspartoyl.L-arginine inhibits platelet aggregation through stimulation of NO release from endothelial cells
Tang, Zhiyu1; Zhao, Ming2; Li, Changling1; Wang, Yinye1; Peng, Shiqi2
关键词polyaspartoyl-l-arginine platelet aggregation rat aortic endothelial cell nitric oxide l-arginine argininosuccinate synthetase citrulline-NO cycle
刊名EUROPEAN JOURNAL OF PHARMACOLOGY
2008-06-24
DOI10.1016/j.ejphar.2008.04.012
588期:1页:41-46
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Pharmacology & Pharmacy
研究领域[WOS]Pharmacology & Pharmacy
关键词[WOS]VASCULAR SMOOTH-MUSCLE ; NITRIC-OXIDE SYNTHESIS ; ARGININOSUCCINATE SYNTHETASE ; RELAXING FACTOR ; L-CITRULLINE ; WHOLE-BLOOD ; ARTERY ; REGENERATION ; PROSTACYCLIN ; TRANSPORT
英文摘要

Polyaspartoyl.L-arginine (PDR) is an inhibitor of platelet aggregation ex vivo but in vitro. This study attempts to elucidate the target cell of PDR action and its action mechanism. PDR (1.7-170 mu g/ml) significantly inhibited platelet aggregation in vitro in the presence of rat aortic endothelial cells (RAEC), NO synthase inhibitor N-nitro-L-arginine methyl ester (I-NAME) inhibited this effect, but it was ineffective in the RAEC absence. Correspondingly, PDR increased NO level in the supernatants of the platelet reactants in RAEC presence, but failed to influence NO level in RAEC absence, and these effects of PDR were more potent than those of L-arginine. Furthermore, PDR markedly elevated the intracellular level of L-arginine, and it (17170 mu g/ml) also augmented L-Citrulline level in RAEC, argininosuccinate lyase (ASL) inhibitor succinate enhanced its effect on L-citrulline but L-NAME weakened it. 170 mu g/ml of PDR slightly increased the L-aspartate level in RAEC, and succinate enhanced this effect. However L-arginine, L-aspartate or the combination of L-arginine and L-aspartate failed to change levels of these amino acids. In addition, PDR (170 mu g/ml) stimulated the expression of argininosuccinate synthetase (ASS) protein. In conclusion, the endothelial cell is direct target cell of PDR′s action; FOR facilitates the entry of L-arginine by serving as a carrier of L-arginine into RAEC; it also supplies aspartic acid and stimulates ASS expression, and then enhances the intracellular citrulline-NO cycle, thus increases the availability of L-arginine and NO synthesis. Therefore the effect of FOR on platelet aggregation is primarily attributed to its stimulation of NO synthesis in endothelial cells; PDR may be a better cardiovascular protective agent than L-arginine. (C) 2008 Elsevier B.V. All rights reserved.

语种英语
WOS记录号WOS:000256861600006
引用统计
被引频次:3[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/67817
专题北京大学药学院
北京大学药学院_分子与细胞药理学系
医学人文研究院/公共教学部_哲学与社会科学系
作者单位1.Peking Univ, Sch Pharmaceut Sci, Dept Mol & Cellular Pharmacol, Beijing 100083, Peoples R China
2.Capital Univ Med Sci, Beijing Key Labs Hydrone & Peptides, Beijing 100069, Peoples R China
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GB/T 7714
Tang, Zhiyu,Zhao, Ming,Li, Changling,et al. Polyaspartoyl.L-arginine inhibits platelet aggregation through stimulation of NO release from endothelial cells[J]. EUROPEAN JOURNAL OF PHARMACOLOGY,2008,588(1):41-46.
APA Tang, Zhiyu,Zhao, Ming,Li, Changling,Wang, Yinye,&Peng, Shiqi.(2008).Polyaspartoyl.L-arginine inhibits platelet aggregation through stimulation of NO release from endothelial cells.EUROPEAN JOURNAL OF PHARMACOLOGY,588(1),41-46.
MLA Tang, Zhiyu,et al."Polyaspartoyl.L-arginine inhibits platelet aggregation through stimulation of NO release from endothelial cells".EUROPEAN JOURNAL OF PHARMACOLOGY 588.1(2008):41-46.
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