Abstract |
β-Amyrin is a pentacyclic triterpene found in various plants and has a variety of biological and pharmacological activities. However, the angiogenic effects of β-amyrin in vascular endothelial cells have not been elucidated. Herein, we investigated the effects of β-amyrin on angiogenesis and evaluated the underlying molecular mechanisms. β-Amyrin treatment had no cytotoxic effect on cultured human umbilical vein endothelial cells (HUVECs). It promoted the formation of tube-like structures and enhanced HUVEC migration and the phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) in HUVECs. Pre-treatment with a PI3 kinase or NOS inhibitor blocked β-amyrin-induced phosphorylation of Akt and eNOS. β-Amyrin treatment significantly induced nitric oxide (NO) production in HUVECs. Furthermore, pre-treatment with a PI3 kinase or NOS inhibitor significantly inhibited β-amyrin-induced tube-like structures formation of vascular endothelial cells and HUVEC migration. These data indicate that β-amyrin-induced angiogenesis in vascular endothelial cells may be mediated by Akt-eNOS signaling-dependent mechanisms. These findings suggest that β-amyrin could be a novel therapeutic agent for ischemic vascular diseases.
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Authors | Masakazu Ishii, Tatsuo Nakahara, Shingo Ikeuchi, Masahiro Nishimura |
Journal | Biochemical and biophysical research communications
(Biochem Biophys Res Commun)
Vol. 467
Issue 4
Pg. 676-82
(Nov 27 2015)
ISSN: 1090-2104 [Electronic] United States |
PMID | 26498523
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2015 Elsevier Inc. All rights reserved. |
Chemical References |
- Nitric Oxide
- Oleanolic Acid
- Nitric Oxide Synthase Type III
- Proto-Oncogene Proteins c-akt
- beta-amyrin
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Topics |
- Endothelium, Vascular
(drug effects, enzymology, physiology)
- Human Umbilical Vein Endothelial Cells
- Humans
- Neovascularization, Physiologic
(drug effects)
- Nitric Oxide
(biosynthesis)
- Nitric Oxide Synthase Type III
(metabolism)
- Oleanolic Acid
(analogs & derivatives, pharmacology)
- Proto-Oncogene Proteins c-akt
(metabolism)
- Signal Transduction
(drug effects)
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