title: Olmesartan inhibits the expression of monocyte chemoattractant protein-1 and tumor necrosis factor-alpha and improves vascular remodeling after vascular injury in mouse.
abstract: OBJECTIVE
  To investigate the neointima formation and the expression of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) in cuff-induced vascular injury in mouse model, and to examine the effect of angiotensin II type 1 receptor (AT1) blocker, olmesartan, on MCP-1 and TNF-alpha expression and consequently vascular remodeling.
  
  
  METHODS
  Vascular injury was induced by polyethylene cuff-placement around the mouse femoral artery. Some mice were treated with AT1 receptor blocker, olmesartan, at the dose of 3 mg.kg(-1).day(-1) with an osmotic minipump. Neointima formation and the proliferation of vascular smooth muscle cells (VSMCs) were measured by morphometric analysis and bromodeoxyuridine (BrdU) incorporation. MCP-1 and TNF-alpha expression was detected by Western blot and immunohistochemical staining.
  
  
  RESULTS
  We observed neointima formation 14 days after cuff placement as well as VSMCs proliferation in the media and neointima. Cuff placement also induced MCP-1 and TNF-alpha expression in the media and neointima that the VSMCs specifically existed. Treatment of mice with olmesartan at a dose of 3 mg.kg(-1).day(-1), which did not influence systolic blood pressure, significantly decreased neointima formation and the proliferation of VSMCs. Olmesartan also inhibited MCP-1 and TNF-alpha expression in the injured arteries.
  
  
  CONCLUSIONS
  Our results demonstrate that blockade of AT1 receptor inhibits MCP-1 and TNF-alpha expression and thereby improves vascular remodeling.
authors.affiliation: Department of Surgery, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China. lizhen1029@hotmail.com
authors.forename: Zhen
authors.initials: Z
authors.lastname: Li
authors.forename: Xiao-dong
authors.initials: XD
authors.lastname: Chen
authors.forename: Shao-kai
authors.initials: SK
authors.lastname: Ni
authors.forename: Jian-wen
authors.initials: JW
authors.lastname: Li
authors.forename: Mu-sheng
authors.initials: MS
authors.lastname: Lin
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western; D002455:Cell Division / Q000187:drug effects* / Q000502:physiology; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000032:analysis*; D004195:Disease Models, Animal; D007093:Imidazoles / Q000494:pharmacology*; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009000:Monocytes / Q000166:cytology / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000166:cytology* / Q000187:drug effects; D018919:Neovascularization, Physiologic / Q000187:drug effects* / Q000502:physiology; D000068557:Olmesartan Medoxomil; D011336:Probability; D012680:Sensitivity and Specificity; D013777:Tetrazoles / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis* / Q000187:drug effects; D017539:Tunica Intima / Q000187:drug effects / Q000473:pathology; D014652:Vascular Diseases / Q000503:physiopathology
chemical_list: D018932:Chemokine CCL2; D007093:Imidazoles; D013777:Tetrazoles; D014409:Tumor Necrosis Factor-alpha; D000068557:Olmesartan Medoxomil