Figure 8

α-santalol inhibits angiogenesis ex vivo and in vivo . (A) Aortic rings were embedded in Matrigel, treated with various concentrations of α-santalol and sunitinib in the presence or absence of VEGF and incubated in supplemented media at 37°C, 5% CO2, for 6 days. The images are representative of three experiments (× 100). (B) Bar graphs showing number of microvessel sprouts treated with α-santalol and sunitinib in the presence or absence of VEGF. Values are mean ± SEM (n = 6) of three independent experiments. ##p < 0.01 VEGF-treated group versus no VEGF-treated group; **p < 0.01; ***p < 0.001 versus VEGF stimulated group. Sterile circular sponge discs were inserted subcutaneously into male Swiss albino mice and treated with α-santalol 14 days. Mice were sacrificed and sponge was excised, (C) photographed (D) weighed (E) Excised sponge was homogenized in Drabkin Reagent to quantify the hemoglobin level. The content of hemoglobin in each implant is expressed as g/dl/per wet tissue. (F) Representative histological sections (5 μm, stained with H &E) of sponge implants. Arrows show the blood vessels in control group. (G) Immunohistochemical staining of sponge with VEGF showed reduced expression of VEGF in the α-santalol treated groups. Arrows show the VEGF staining. Levels of VEGF were further quantified by ELISA and expressed as pg/mg wet tissue. (H) Immunohistochemical staining of sponge with CD31. Sections from the sponge tissue that were either untreated or -treated were incubated with anti-CD31 overnight at 4°C and stained with ABC-reagent according to the manufacturers protocol and percent microvessel density was calculated. Arrows show the blood vessels. Values are mesan ± SEM (n = 6) of three independent experiments. *p < 0.05; **p < 0.01; ***p < 0.001 versus control group. S: sponge matrix; Scale bar: 100 μM.