UM
Dl-3n-butylphthalide promotes angiogenesis via the extracellular signal-regulated kinase 1/2 and phosphatidylinositol 3-kinase/akt-endothelial nitric oxide synthase signaling pathways
Lu X.-L.1; Luo D.1; Yao X.-L.1; Wang G.-L.5; Liu Z.-Y.1; Li Z.-X.5; Li W.1; Chang F.-J.1; Wen L.2; Lee S.M.-Y.4; Zhang Z.-J.4; Li L.1; Zeng J.-S.1; Huang R.-X.1; Pei Z.1; Ou J.-S.1
2012-04-01
Source PublicationJournal of Cardiovascular Pharmacology
ISSN01602446 15334023
Volume59Issue:4Pages:352-362
AbstractWe have previously demonstrated that dl-3n-butylphthalide (NBP) has a potential angiogenic activity. In this study, we investigated the angiogenic effect of NBP and the molecular mechanisms underlying NBP-mediated angiogenesis. Zebrafish embryos and human umbilical vein endothelial cells were treated with various doses of NBP and several signaling pathway inhibitors. NBP induced ectopic subintestinal vessel production in zebrafish embryos and induced invasion, migration, and endothelial cell tube formation of human umbilical vein endothelial cells in a dose-dependent manner. These NBP-induced angiogenic effects were partially suppressed by SU5402, a fibroblast growth factor receptor 1 inhibitor; U0126, an extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor; LY294002, a phosphatidylinositol 3-kinase inhibitor; 1L6-hydroxymethyl-chiro-inositol-2-(R)-2-O-methyl-3-O-octadecyl-sn- glycerocarbonate, an Akt inhibitor; cavtratin, an endothelial nitric oxide synthase (eNOS) inhibitor and completely inhibited by a combination of U0126 and LY294002. NBP enhanced phosphorylation of ERK1/2 and fibroblast growth factor receptor 2 expression, which were inhibited by U0126. NBP increased the phosphorylation of Akt and eNOS at serine 1177, which was blocked by LY294002. NBP-stimulated nitric oxide production, which was reduced by LY294002. Our data demonstrated that (1) NBP promoted angiogenesis and (2) the angiogenic effects of NBP were mediated by the ERK1/2 and phosphatidylinositol 3-kinase/Akt-eNOS signaling pathways. Our findings suggest that NBP could be a novel agent for therapeutic angiogenesis in ischemic diseases. © 2012 by Lippincott Williams & Wilkins.
Keywordangiogenesis dl-3n-butylphthalide endothelial nitric oxide synthase extracellular signal-regulated kinase 1/2 phosphatidylinositol 3-kinase zebrafish
DOI10.1097/FJC.0b013e3182443e74
URLView the original
Language英語
Fulltext Access
Citation statistics
Cited Times [WOS]:21   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionUniversity of Macau
Affiliation1.Ministry of Health of People's Republic of China
2.Sun Yat-Sen University
3.Key Laboratory of Functional Molecules from Oceanic Microorganisms
4.University of Macau
5.Sun Yat-Sen University, Zhongshan School of Medicine
Recommended Citation
GB/T 7714
Lu X.-L.,Luo D.,Yao X.-L.,et al. Dl-3n-butylphthalide promotes angiogenesis via the extracellular signal-regulated kinase 1/2 and phosphatidylinositol 3-kinase/akt-endothelial nitric oxide synthase signaling pathways[J]. Journal of Cardiovascular Pharmacology,2012,59(4):352-362.
APA Lu X.-L..,Luo D..,Yao X.-L..,Wang G.-L..,Liu Z.-Y..,...&Ou J.-S..(2012).Dl-3n-butylphthalide promotes angiogenesis via the extracellular signal-regulated kinase 1/2 and phosphatidylinositol 3-kinase/akt-endothelial nitric oxide synthase signaling pathways.Journal of Cardiovascular Pharmacology,59(4),352-362.
MLA Lu X.-L.,et al."Dl-3n-butylphthalide promotes angiogenesis via the extracellular signal-regulated kinase 1/2 and phosphatidylinositol 3-kinase/akt-endothelial nitric oxide synthase signaling pathways".Journal of Cardiovascular Pharmacology 59.4(2012):352-362.
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Google Scholar
Similar articles in Google Scholar
[Lu X.-L.]'s Articles
[Luo D.]'s Articles
[Yao X.-L.]'s Articles
Baidu academic
Similar articles in Baidu academic
[Lu X.-L.]'s Articles
[Luo D.]'s Articles
[Yao X.-L.]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Lu X.-L.]'s Articles
[Luo D.]'s Articles
[Yao X.-L.]'s Articles
Terms of Use
No data!
Social Bookmark/Share
All comments (0)
No comment.
 

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.