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60%食用乙醇提取物可抑制血管内皮生长因子诱导的血管生成。

A 60% Edible Ethanolic Extract of Inhibits Vascular Endothelial Growth Factor-Induced Angiogenesis.

机构信息

College of Veterinary Medicine and Institute of Veterinary Science, Kangwon National University, Chuncheon, Gangwon-do 24341, Korea.

Department of Biotechnology and Bioengineering, Kangwon National University, Chuncheon, Gangwon-do 24341, Korea.

出版信息

Molecules. 2021 Feb 3;26(4):781. doi: 10.3390/molecules26040781.

DOI:10.3390/molecules26040781
PMID:33546250
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7913375/
Abstract

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. 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 (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.

摘要

由于异常血管生成与各种疾病的恶化有关,因此精确控制血管生成至关重要。血管内皮生长因子(VEGF)是最著名的血管生成因子,它与血管内皮生长因子受体(VEGFR)结合,激活各种信号通路,并介导血管生成。因此,通过抑制血管生成,阻断 VEGF 诱导的血管生成反应相关信号通路可能缓解各种疾病症状。是一种安全的天然产物,传统上被食用,但它对内皮细胞(ECs)的作用及其作用机制尚不清楚。在本研究中,我们专注于 60%食用乙醇提取物对血管生成的影响。U60E 抑制了 VEGF 介导的 ECs 的增殖、管形成和迁移能力。从机制上讲,U60E 通过阻断 VEGF 激活的蛋白激酶 B 信号通路来抑制内皮型一氧化氮合酶的激活和一氧化氮的产生,从而抑制 ECs 的增殖、管形成和迁移。这些结果表明,U60E 可能是一种潜在的安全治疗剂,通过抑制 VEGF 诱导的血管生成,能够抑制促血管生成疾病。

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