A 60% Edible Ethanolic Extract of Ulmus davidiana Inhibits Vascular Endothelial Growth Factor-Induced Angiogenesis
| Autor: | Kwang-Hyun Park, Myung-Bok Wie, Jeongho Park, Sun-Eun Choi, Hyun-Ouk Kim, Jang-Hyuk Yun |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Angiogenesis
proliferation Pharmaceutical Science tube formation migration Analytical Chemistry Nitric oxide lcsh:QD241-441 03 medical and health sciences chemistry.chemical_compound angiogenesis 0302 clinical medicine Ulmus davidiana lcsh:Organic chemistry Drug Discovery Physical and Theoretical Chemistry 030304 developmental biology Tube formation 0303 health sciences biology Chemistry Organic Chemistry biology.organism_classification Vascular endothelial growth factor Endothelial stem cell Chemistry (miscellaneous) 030220 oncology & carcinogenesis Protein kinase B signaling Cancer research endothelial cell Molecular Medicine Signal transduction |
| Zdroj: | Molecules Volume 26 Issue 4 Molecules, Vol 26, Iss 781, p 781 (2021) |
| ISSN: | 1420-3049 |
| DOI: | 10.3390/molecules26040781 |
| Popis: | As abnormal angiogenesis is associated with exacerbation of various diseases, precise control over angiogenesis is imperative. Vascular endothelial growth factor (VEGF), the most well-known angiogenic factor, binds to VEGF receptor (VEGFR), activates various signaling pathways, and mediates angiogenesis. Therefore, blocking the VEGF-induced angiogenic response-related signaling pathways may alleviate various disease symptoms through inhibition of angiogenesis. Ulmus davidiana is a safe natural product that has been traditionally consumed, but its effects on endothelial cells (ECs) and the underlying mechanism of action are unclear. In the present study, we focused on the effect of a 60% edible ethanolic extract of U. davidiana (U60E) on angiogenesis. U60E inhibited the VEGF-mediated proliferation, tube formation, and migration ability of ECs. Mechanistically, U60E inhibited endothelial nitric oxide synthase activation and nitric oxide production by blocking the protein kinase B signaling pathway activated by VEGF and consequently inhibiting proliferation, tube formation, and migration of ECs. These results suggest that U60E could be a potential and safe therapeutic agent capable of suppressing proangiogenic diseases by inhibiting VEGF-induced angiogenesis. |
| Databáze: | OpenAIRE |
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