β-Amyrin induces angiogenesis in vascular endothelial cells through the Akt/endothelial nitric oxide synthase signaling pathway

Abstract

β-Amyrin is a pentacyclic triterpene found in various plants and has a variety of biological and pharmacological activities. However, the angiogenic effects of β-amyrin in vascular endothelial cells have not been elucidated. Herein, we investigated the effects of β-amyrin on angiogenesis and evaluated the underlying molecular mechanisms. β-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 β-amyrin-induced phosphorylation of Akt and eNOS. β-Amyrin treatment significantly induced nitric oxide (NO) production in HUVECs. Furthermore, pre-treatment with a PI3 kinase or NOS inhibitor significantly inhibited β-amyrin-induced tube-like structures formation of vascular endothelial cells and HUVEC migration. These data indicate that β-amyrin-induced angiogenesis in vascular endothelial cells may be mediated by Akt-eNOS signaling-dependent mechanisms. These findings suggest that β-amyrin could be a novel therapeutic agent for ischemic vascular diseases.

Keywords: Angiogenesis; Endothelial cell; NO; eNOS; β-Amyrin.