beta-Amyrin is a pentacyclic triterpene found in various plants and has a variety of biological and pharmacological activities. However, the angiogenic effects of beta-amyrin in vascular endothelial cells have not been elucidated. Herein, we investigated the effects of beta-amyrin on angiogenesis and evaluated the underlying molecular mechanisms. beta-Amyrin treatment had no cytotoxic effect on cultured human umbilical vein endothelial cells (HUVECs). It promoted the formation of tube-like structures and enhanced HUVEC migration and the phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) in HUVECs. Pre-treatment with a PI3 kinase or NOS inhibitor blocked beta-amyrin-induced phosphorylation of Akt and eNOS. beta-Amyrin treatment significantly induced nitric oxide (NO) production in HUVECs. Furthermore, pre-treatment with a PI3 kinase or NOS inhibitor significantly inhibited beta-amyrin-induced tube-like structures formation of vascular endothelial cells and HUVEC migration. These data indicate that beta-amyrin-induced angiogenesis in vascular endothelial cells may be mediated by Akt-eNOS signaling-dependent mechanisms. These findings suggest that beta-amyrin could be a novel therapeutic agent for ischemic vascular diseases. (C) 2015 Elsevier Inc. All rights reserved.