Fig. 3

Ginsenoside F1 promoted angiogenesis in vitro, ex vivo and in vivo. (A–B) GF1 increased the tube formation capabilities of HUVECs and HBMECs. HUVECs or HBMECs were seeded in Matrigel-coated 96-well plates and treated with or without GF1 (20 and 40 μM) for 6 h. VEGF (80 ng/mL) served as the positive control. The endothelial tubes were observed and photographed. Quantification of the number of tubes is shown. (C–D) GF1 increased vessel sprouting in the rat aorta rings. Rat aortic rings were treated with or without GF1 (20 and 40 μM) for 48 h. VEGF (100 ng/mL) served as the positive control. Vessel sprouting was observed and photographed at 0 and 48 h. Quantification of the number of sprouting vessels is shown. (E–F) GF1 stimulated neovascularization in the CAM. Fertilized eggs were treated with or without GF1 (20 and 40 μM) for 48 h. VEGF (100 ng/mL) served as the positive control. The neovessels were observed and captured after 48 h. Quantification of the number of capillaries is shown. (G)GF1 rescued the VRI-induced vessel defect in zebrafish. Zebrafish were treated with VRI (axitinib, 1 μM) at 24 hpf for 6 h, followed by treatment with 0.1% DMSO (v/v), VEGF (200 ng/mL), or GF1 (20 and 40 μM) for 24 or 48 h. The ISVs were observed and photographed at 24 and 48 h. Representative images are shown; scale bars: 200 μm (A), 500 μm (C and G), and 1 mm (E). The data are presented as mean ± SEM (n = 3). ^*P < 0.05, ^**P < 0.01, and ^***P < 0.001 compared with the control group.