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. 2022 Sep 1;12(3):20–30. doi: 10.37796/2211-8039.1343

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This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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Fig. 2 — Akt, eNOS, NF-κB and MAPK/ERK signaling cascades involve in 11,12-EET-mediated neovasculogenesis. hEPCs were treated with wortmannin (10 μM), PD098059 (10 μM), Bay-11-7082 (1 μM) and l-NAME (0.1 mM) in the presence of 11,12-EET (50 nM) for 8 h until the analysis of neovasculogenesis (A). The values represent mean ± SD for the quantitative results (B). A single asterisk (*) indicates a statistical difference in comparison with the 11,12-EET-treated group (P < 0.05). Double asterisks (**) indicate a statistical difference in comparison with the 11,12-EET-untreated control group (P < 0.05). Viability analysis of hEPCs was performed under the same treatments. The proliferation index is provided as mean ± SD (C). Different letters represent significant differences of proliferation index among subgroups.