Ginkgolide B promotes cell growth in endothelial progenitor cells through miR-126 and the Akt signaling pathway.

Ginkgolide B is one of the components extracted from Folium Ginkgo. It is a natural antagonist of platelet‑activating factor receptor and has multiple pharmacological applications. In the present study, the effect of ginkgolide B on the proliferation of endothelial progenitor cells (EPCs) was examined, as well as its potential underlying mechanism. EPCs were cultured in various concentrations of ginkgolide B (0, 1.25, 5, 20, 80 or 160 µg/ml) for 24 or 48 h and then numbers of viable cells, apoptosis rate and caspace‑3 activity were measured. The results demonstrated that ginkgolide B treatment effectively promoted EPC growth, and suppressed cell apoptosis and caspase‑3 activity compared with control cells. In addition, ginkgolide B treatment significantly induced the expression of miR‑126, vascular endothelial growth factor and endothelial nitric oxide synthase, while it increased phosphorylation of AKT serine/threonine kinase 1 (Akt) and of p38 mitogen‑activated protein kinase in EPCs. The present study therefore demonstrated that ginkgolide B promoted cell growth in EPCs through overexpression of miR‑126 and activation of the Akt signaling pathway.