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. 2017 Jul 14;7:5376. doi: 10.1038/s41598-017-05512-9

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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AE-AS inhibited the angiogenesis in CAM and Matrigel plugs. The vessel angiogenesis in CAM was determined and photographed, and the vascular branch was quantified by an angiogenesis-measuring software (A). Data was expressed as mean ± SEM (n = 5). **P < 0.01 versus hypoxia + T24-treated alone group. The functional vasculature formation induced by VEGF (100 ng) in Matrigel plugs was photographed and stained with H&E (200×). The infiltrating microvessels with intact RBC were quantified by manual counting using high power fields (200×) **P < 0.01, ***P < 0.001 versus VEGF-treated alone group.