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Antiangiogenic Activity of Acer tegmentosum Maxim Water Extract in Vitro and in Vivo

  • Kim, Eok-Cheon (Division of Biological Science and Technology and Yonsei-Fraunhofer Medical Device Lab., College of Science and Technology, Yonsei University) ;
  • Kim, So Hun (Division of Endocrinology and Metabolism, Department of Internal Medicine, Inha University School of Medicine) ;
  • Piao, Shan-Ji (Qingdao Endocrine & Diabetes Hospital) ;
  • Kim, Tack-Joong (Division of Biological Science and Technology and Yonsei-Fraunhofer Medical Device Lab., College of Science and Technology, Yonsei University) ;
  • Bae, Kiho (Division of Biological Science and Technology and Yonsei-Fraunhofer Medical Device Lab., College of Science and Technology, Yonsei University) ;
  • Kim, Han Sung (Department of Biomedical Engineering, Institute of Medical Engineering and Yonsei-Fraunhofer Medical Device Laboratory, Yonsei University) ;
  • Hong, Soon-Sun (Department of Biomedical Sciences, College of Medicine, Inha University) ;
  • Lee, Byoung Ick (Department of Obstetrics & Gynecology, Inha University College of Medicine) ;
  • Nam, Moonsuk (Division of Endocrinology and Metabolism, Department of Internal Medicine, Inha University School of Medicine)
  • Received : 2015.03.06
  • Accepted : 2015.04.01
  • Published : 2015.07.10

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.

Keywords

Acknowledgement

Supported by : Inha University, Ministry of Health and Welfare

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