Objective: To investigate the neointima formation and the expression of monocyte chemoattractant protein 1 (MCP 1) and tumor necrosis factor α (TNF α) in cuff induced vascular injury in mouse model, and to examine the effect of angiotensin II type 1 receptor (AT 1) blocker, olmesartan, on MCP 1 and TNF α expression and consequently vascular remodeling. Methods: Vascular injury was induced by polyethylene cuff placement around the mouse femoral artery. Some mice were treated with AT 1 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 α 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 α 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 α expression in the injured arteries. Conclusions: Our results demonstrate that blockade of AT 1 receptor inhibits MCP 1 and TNF α expression and thereby improves vascular remodeling. Objective: To investigate the neointima formation and the expression of monocyte chemoattractant protein 1 (MCP 1) and tumor necrosis factor α (TNFα) in cuff induced vascular injury in mouse model, and to examine the effect of angiotensin II type 1 receptor (AT 1) blocker, olmesartan, on MCP 1 and TNF α expression andrized vascular remodeling. Methods: Vascular injury was induced by polyethylene cuff placement around the mouse femoral artery. Some mice were treated with AT 1 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 α expression was detected by Western blot and immunohistochemical staining. Results: We observed neointima formation for 14 days after cuff placement as well as VSMCs proliferation in the media and neointima. Cuff Treatment of mice with olmesartan at a dose of 3 mg · kg -1 · day -1, which did not influence systolic blood pressure, decreased significantly Neointima formation and the proliferation of VSMCs. Olmesartan also inhibited MCP 1 and TNF α expression in the injured arteries. Conclusions: Our results demonstrate that blockade of AT 1 receptor inhibits MCP 1 and TNF α expression and so improves vascular remodeling.