الفهرس 
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Abstract
Restenosis after successful coronary intervention remains a major limitation to the long-term outcome of this procedure (Leimgruber et al., 1996). Intimal hyperplasia is one of the major mechanisms responsible for postangioplasty restenosis (Post et al., 2004).
The formation of intimal hyperplasia is mainly due to the phenotypic conversion and proliferation of smooth muscle cells as well as the accumulation of ac¬tivated macrophages and foam cells (Hanke et al., 2004-Chen et al., 2007).
Activated macrophages and smooth muscle cells may express a number of cytokines, growth factors, and chemoattractant proteins, which are involved in the vessel wall remodeling, and could further exacerbate the progression of restenotic lesions (Schwartz et al., 2005).
The monocyte chemotactic protein-l (MCP-1) is an important mediator of monocyte recruitment into the vascular wall at sites of active inflammation or injury. It is secreted by stimulated human lymphocytes, endothelial cells, fibroblasts, monocytes, and smooth muscle cells in vitro (Kaczmarek et al., 1995-Valente et al., 1998-Strieter et al., 1999-Yoshimura et al., 1999-Rollins et al., 2000).
Increased levels of MCP-1 have been demonstrated in some animal models of postangioplasty restenosis, indicating that it may play an important role in the pathogenesis of vascular lesion formation ( Wysocki et al., 2006-Merritt et al., 2007 ).
To evaluate the possibility of SM on the prevention of arterial restenosis after angioplasty, the effect of SM on intimal thickening of the air-injured carotid artery of rats was studied. It was found that the maximal intimal thickness of the injured arteries was much thinner in the treatment group than that in the control group indicating that SM could prevent experimental restenosis in rat model. Findings from in vitro study indicate that the beneficial effect of SM on restenosis might be due to its inhibition on the proliferation of smooth muscle cells (Zhou et al., 2006).
In another study, the effects of SM on neointimal hyperplasia and MCP-I expression after balloon injury were evaluated. Male New Zealand while rabbits were fed a 2% cholesterol diet together with daily SM (4.8 g/kg body weight) treatment or without SM as a control for 6 weeks. The plasma cholesterol levels were lowered in the SM group. The neointimal hyperplasia in abdominal aortas was significantly inhibited in the SM group when compared with the control group. SM treatment significantly reduced MCP-I mRNA and protein expression in balloon-injured abdominal aorta. Results from this study implied that SM might inhibit the expression of MCP-I and thereby reduce the intimal response after balloon injury of aortas in cholesterol-fed rabbits, suggesting that SM treatment may offer some protection against postangioplasty restenosis (Chen et al., 2007).
Apoptosis has been suggested to participate in stabilizing cell number in restenosis.
To determine whether SM affects vascular apoptosis, frequency of apoptotic cell death in atherosclerotic plaques and in restenotic lesions of cholesterol-fed and endothelial denudation (HC-ED) rabbits were examined. Apoptosis and associated cell types were examined in serial paraffin sections by in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL assay) and immunohistochemistry.
The expression of p53 an apoptosis-related protein, was also examined. Apoptosis was mainly detected in the neointima of animals with endothelial denudation. The per¬centage of apoptotic cells in the SM-treated group (68.5 ± 5.9%) was significantly higher than that of the control (0%) and HC-ED (46.1 ± 5.4%) groups. The SM treatment markedly reduced the thickness of the neointima which was mainly composed of smooth muscle cells with few macrophages.