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学科主题: 药学
题名:
Polyaspartoyl.L-arginine inhibits platelet aggregation through stimulation of NO release from endothelial cells
作者: 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
发表日期: 2008-06-24
DOI: 10.1016/j.ejphar.2008.04.012
卷: 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
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/67817
Appears in Collections:北京大学药学院_期刊论文

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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

Recommended Citation:
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.
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