BACKGROUND: The proliferation and migration of vascular endothelial cells (VECs) plays a vital role in angiogenesis, a process that influences plaque vulnerability in human atherosclerosis. Luteolin is a type of flavonoid that has shown a positive effect on the morbidity and mortality of cardiovascular diseases. However, it remains unclear whether this compound has a protective effect against the proliferation and migration of human umbilical vein endothelial cells (HUVECs) induced by angiotensin II (AngII). METHODS AND RESULTS: HUVECs were treated with different concentrations of luteolin for varying lengths of time. Analysis using methyl thiazolyl tetrazolium and 5-ethynyl-2'-deoxyuridine revealed that 25 μmol/L luteolin had a particularly inhibitory effect on the AngII-induced proliferation of HUVECs. A Transwell chamber was then used to assay the migration of HUVECs in the presence of 12.5 μmol/L luteolin. The results showed that the migration of AngII-induced HUVECs was also inhibited by luteolin. Further investigations showed that the phosphorylation levels of Src, p-Akt (308), and p-Akt (473) in the group treated with both luteolin and AngII were significantly lower than those of the group treated with only AngII. CONCLUSIONS: The inhibitory effects of luteolin on the proliferation and migration of VECs stimulated by AngII are mediated through the downregulation of the PI3K/Akt signaling pathway.
BACKGROUND: The proliferation and migration of vascular endothelial cells (VECs) plays a vital role in angiogenesis, a process that influences plaque vulnerability in humanatherosclerosis. Luteolin is a type of flavonoid that has shown a positive effect on the morbidity and mortality of cardiovascular diseases. However, it remains unclear whether this compound has a protective effect against the proliferation and migration of human umbilical vein endothelial cells (HUVECs) induced by angiotensin II (AngII). METHODS AND RESULTS: HUVECs were treated with different concentrations of luteolin for varying lengths of time. Analysis using methyl thiazolyl tetrazolium and 5-ethynyl-2'-deoxyuridine revealed that 25 μmol/L luteolin had a particularly inhibitory effect on the AngII-induced proliferation of HUVECs. A Transwell chamber was then used to assay the migration of HUVECs in the presence of 12.5 μmol/L luteolin. The results showed that the migration of AngII-induced HUVECs was also inhibited by luteolin. Further investigations showed that the phosphorylation levels of Src, p-Akt (308), and p-Akt (473) in the group treated with both luteolin and AngII were significantly lower than those of the group treated with only AngII. CONCLUSIONS: The inhibitory effects of luteolin on the proliferation and migration of VECs stimulated by AngII are mediated through the downregulation of the PI3K/Akt signaling pathway.