中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Pseudolarix acid B inhibits angiogenesis by antagonizing the vascular endothelial growth factor-mediated anti-apoptotic effect

文献类型:期刊论文

作者Tan, WF; Zhang, XW; Li, MH; Yue, JM; Chen, Y; Lin, LP; Ding, J
刊名EUROPEAN JOURNAL OF PHARMACOLOGY
出版日期2004-09-24
卷号499期号:3页码:219-228
ISSN号0014-2999
关键词pseudolarix acid B angiogenesis umbilical vein endothelial cell apoptosis VEGF KDR (Human)
DOI10.1016/j.ejphar.2004.07.063
文献子类Article
英文摘要Angiogenesis is controlled by a number of growth factors, including vascular endothelial growth factor (VEGF). In this study, pseudolarix acid 13, isolated from the traditional Chinese medicinal plant Pseudolarix kaempferi and originally identified as an early pregnancy-terminating agent, was evaluated for its potential as an angiogenesis inhibitor, using in vitro and in vivo models. After exposure to pseudolarix acid B 0.625-5 muM for 72 h, the proliferation of human umbilical vein endothelial cells was significantly inhibited. Pseudolarix acid B 0.313-2.5 muM for 24 h potently blocked the VEGF-induced tube formation of human umbilical vein endothelial cells in a dose-dependent manner. Matrigel plug assays disclosed that pseudolarix acid B reduced angiogenesis induced by VEGF in vivo. In addition, pseudolarix acid B antagonized VEGF-mediated anti-apoptotic effects on serum-deprived human umbilical vein endothelial cells and increased apoptosis of endothelial cells induced by VEGF in Matrigel plug assays. Moreover, pseudolarix acid B significantly inhibited VEGF-induced tyrosine phosphorylation of kinase insert domain-containing receptor/fetal liver kinase-1 (KDR/flk-1), in correlation with a marked decrease in the phosphorylation of Akt and extracellular signal-regulated kinases (ERK). These findings collectively suggest that pseudolarix acid B possesses anti-angiogenic activity. One of the main anti-angiogenesis mechanisms of pseudolarix acid B may involve antagonism of the VEGF-mediated anti-apoptosis effect via inhibition of KDR/flk-1, ERK1/2, and Akt phosphorylation in endothelial cells. (C) 2004 Elsevier B.V. All rights reserved.
WOS关键词SURVIVAL FACTOR ; CELL SURVIVAL ; TUMOR ; AGENTS ; KAEMPFERI ; VESSELS ; TARGET ; CANCER
WOS研究方向Pharmacology & Pharmacy
语种英语
出版者ELSEVIER SCIENCE BV
WOS记录号WOS:000224232300001
源URL[http://119.78.100.183/handle/2S10ELR8/274019]  
专题药理学第一研究室
中科院受体结构与功能重点实验室
新药研究国家重点实验室
通讯作者Ding, J
作者单位1.Chinese Acad Sci, Div Anti Tumor Pharmacol, State Key Lab Drug Res, Shanghai Inst Mat Med,Inst Biol Sci, Shanghai 201203, Peoples R China
2.Chinese Acad Sci, Grad Sch, Shanghai 201203, Peoples R China
3.Chinese Acad Sci, Div Phytochem, Shanghai Inst Mat Med, Inst Biol Sci, Shanghai 201203, Peoples R China
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GB/T 7714
Tan, WF,Zhang, XW,Li, MH,et al. Pseudolarix acid B inhibits angiogenesis by antagonizing the vascular endothelial growth factor-mediated anti-apoptotic effect[J]. EUROPEAN JOURNAL OF PHARMACOLOGY,2004,499(3):219-228.
APA Tan, WF.,Zhang, XW.,Li, MH.,Yue, JM.,Chen, Y.,...&Ding, J.(2004).Pseudolarix acid B inhibits angiogenesis by antagonizing the vascular endothelial growth factor-mediated anti-apoptotic effect.EUROPEAN JOURNAL OF PHARMACOLOGY,499(3),219-228.
MLA Tan, WF,et al."Pseudolarix acid B inhibits angiogenesis by antagonizing the vascular endothelial growth factor-mediated anti-apoptotic effect".EUROPEAN JOURNAL OF PHARMACOLOGY 499.3(2004):219-228.

入库方式: OAI收割

来源:上海药物研究所

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