title: Luteolin inhibits angiotensin II-induced human umbilical vein endothelial cell proliferation and migration through downregulation of Src and Akt phosphorylation.
abstract: 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).
  
  
  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.
authors.affiliation: Institute of Cardiovascular Disease Research, Xuzhou Medical College, Jiangsu, China.
authors.forename: Manyi
authors.initials: M
authors.lastname: Zhu
authors.forename: Dan
authors.initials: D
authors.lastname: Chen
authors.forename: Dongye
authors.initials: D
authors.lastname: Li
authors.forename: Hong
authors.initials: H
authors.lastname: Ding
authors.forename: Tian
authors.initials: T
authors.lastname: Zhang
authors.forename: Tongda
authors.initials: T
authors.lastname: Xu
authors.forename: Yanbin
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D002465:Cell Movement / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects*; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation / Q000187:drug effects; D004730:Endothelium, Vascular / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D047311:Luteolin / Q000494:pharmacology*; D009389:Neovascularization, Pathologic / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors; D014471:Umbilical Veins / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D019061:src-Family Kinases / Q000378:metabolism*
chemical_list: D000804:Angiotensin II; D019869:Phosphatidylinositol 3-Kinases; D019061:src-Family Kinases; D051057:Proto-Oncogene Proteins c-akt; D047311:Luteolin