PMID- 14728822
OWN - NLM
STAT- MEDLINE
DCOM- 20040310
LR  - 20161020
IS  - 1008-1275 (Print)
IS  - 1008-1275 (Linking)
VI  - 7
IP  - 1
DP  - 2004 Feb
TI  - Olmesartan inhibits the expression of monocyte chemoattractant protein-1 and 
      tumor necrosis factor-alpha and improves vascular remodeling after vascular 
      injury in mouse.
PG  - 56-61
AB  - 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.
FAU - Li, Zhen
AU  - Li Z
AD  - Department of Surgery, Affiliated Hospital of Guangdong Medical College, 
      Zhanjiang 524001, China. lizhen1029@hotmail.com
FAU - Chen, Xiao-dong
AU  - Chen XD
FAU - Ni, Shao-kai
AU  - Ni SK
FAU - Li, Jian-wen
AU  - Li JW
FAU - Lin, Mu-sheng
AU  - Lin MS
LA  - eng
PT  - Journal Article
PL  - China
TA  - Chin J Traumatol
JT  - Chinese journal of traumatology = Zhonghua chuang shang za zhi
JID - 100886162
RN  - 0 (Chemokine CCL2)
RN  - 0 (Imidazoles)
RN  - 0 (Tetrazoles)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 6M97XTV3HD (Olmesartan Medoxomil)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Blotting, Western
MH  - Cell Division/*drug effects/physiology
MH  - Cells, Cultured
MH  - Chemokine CCL2/*analysis
MH  - Disease Models, Animal
MH  - Imidazoles/*pharmacology
MH  - Immunohistochemistry
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Monocytes/cytology/drug effects
MH  - Muscle, Smooth, Vascular/*cytology/drug effects
MH  - Neovascularization, Physiologic/*drug effects/physiology
MH  - Olmesartan Medoxomil
MH  - Probability
MH  - Sensitivity and Specificity
MH  - Tetrazoles/*pharmacology
MH  - Tumor Necrosis Factor-alpha/*analysis/drug effects
MH  - Tunica Intima/drug effects/pathology
MH  - Vascular Diseases/physiopathology
EDAT- 2004/01/20 05:00
MHDA- 2004/03/11 05:00
CRDT- 2004/01/20 05:00
PHST- 2004/01/20 05:00 [pubmed]
PHST- 2004/03/11 05:00 [medline]
PHST- 2004/01/20 05:00 [entrez]
PST - ppublish
SO  - Chin J Traumatol. 2004 Feb;7(1):56-61.