Antiangiogenic Activity of Acer tegmentosum Maxim Water Extract in Vitro and in Vivo.
10.3346/jkms.2015.30.7.979
- Author:
Eok Cheon KIM
1
;
So Hun KIM
;
Shan Ji PIAO
;
Tack Joong KIM
;
Kiho BAE
;
Han Sung KIM
;
Soon Sun HONG
;
Byoung Ick LEE
;
Moonsuk NAM
Author Information
1. Division of Biological Science and Technology and Yonsei-Fraunhofer Medical Device Lab., College of Science and Technology, Yonsei University, Wonju, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Angiogenesis;
Acer tegmentosum Maxim;
Vascular Endothelial Growth Factor A;
p44/42 MAP Kinase
- MeSH:
Acer/*metabolism;
Angiogenesis Inhibitors/*pharmacology;
Animals;
Cell Line, Tumor;
Cell Movement/drug effects;
Cell Proliferation/drug effects;
Cell Survival;
Extracellular Signal-Regulated MAP Kinases/*metabolism;
Hep G2 Cells;
Human Umbilical Vein Endothelial Cells/*drug effects;
Humans;
MAP Kinase Signaling System/drug effects;
Mice;
Mice, Inbred C57BL;
Mitogen-Activated Protein Kinase 1/metabolism;
Neoplasm Invasiveness/pathology;
Neovascularization, Pathologic/*drug therapy/prevention & control;
Nitric Oxide Synthase Type III/metabolism;
Phosphorylation/drug effects;
Plant Extracts/pharmacology;
Rats;
Rats, Sprague-Dawley;
Transcription Factors/metabolism;
Vascular Endothelial Growth Factor A/antagonists & inhibitors/metabolism
- From:Journal of Korean Medical Science
2015;30(7):979-987
- CountryRepublic of Korea
- Language:English
-
Abstract:
Angiogenesis, the formation of new blood vessels, is critical for tumor growth and metastasis. Notably, tumors themselves can lead to angiogenesis by inducing vascular endothelial growth factor (VEGF), which is one of the most potent angiogenic factors. Inhibition of angiogenesis is currently perceived as one of the most promising strategies for the blockage of tumor growth. In this study, we investigated the effects of Acer tegmentosum maxim water extract (ATME) on angiogenesis and its underlying signal mechanism. We studied the antiangiogenic activity of ATME by using human umbilical vein endothelial cells (HUVECs). ATME strongly inhibited VEGF-induced endothelial cell proliferation, migration, invasion, and tube formation, as well as vessel sprouting in a rat aortic ring sprouting assay. Moreover, we found that the p44/42 mitogen activated protein (MAP) kinase signaling pathway is involved in the inhibition of angiogenesis by ATME. Moreover, when we performed the in vivo matrigel plug assay, VEGF-induced angiogenesis was potently reduced when compared to that for the control group. Taken together, these results suggest that ATME exhibits potent antiangiogenic activity in vivo and in vitro and that these effects are regulated by the extracellular regulated kinase (ERK) pathway.
