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. 2017 Dec 18;26(10):1636–1647. doi: 10.1177/0963689717724792

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© The Author(s) 2017

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Fig. 2. — S-allylcysteine (SAC) modulates neovasculogenesis through PI3-K/Akt/endothelial nitric oxide synthase signaling pathways in endothelial progenitor cells (EPCs). (A) EPCs were treated with wortmannin (10 μM; panel c, d) or L-NAME (0.3 mM; panel e, f) in the absence or presence of 100 μM of SAC until the analysis of neovascularization for 8 h, respectively. (B) The values (mean ± standard deviation [SD]) are represented as neovasculogenesis index (folds of tube formation in comparison with the untreated control group) in 8 randomly selected fields in each culture dish. A different letter represents a statistically significant difference among different subgroups (P < 0.05). (C) Cell viability was measured by using 3-[4,5-dimethhylthiaoly]-2,5-diphenyltetrazolium bromide analysis. The proliferation index is represented as the mean ± SD. No significant difference was found (P > 0.05).