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Atorvastatin Calcium on the Rat Carotid Artery Intimal Hyperplasia After Balloon Injury and the Expression of MMP-2

Author: ZhuYongFeng
Tutor: SiZhongYi
School: Liaoning Medical
Course: Surgery
Keywords: Arterial injury Vascular stenosis Intimal hyperplasia Apoptosis Matrix metalloproteinase
CLC: R965
Type: Master's thesis
Year: 2011
Downloads: 26
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Abstract


The purpose of application of rat carotid artery intimal injury animal model, observed at different time points VSMCs proliferation and vascular remodeling explore vascular stenosis pathogenesis and explore the vascular endothelial injury Hou Atuo cutting Atorvastatin calcium on the proliferation of VSMCs suppression role after rat carotid artery injury MMP-2, Bax, Bcl-2 protein. Methods Male Sprague Dawley rats were randomly divided into: sham group, injury group and injury Atto Atorvastatin calcium treatment group. HE staining observed 3,7,14,28 days after vascular injury vascular morphology changes, with the help of computer image analysis system to calculate each group rat carotid artery neointimal thickness, neointimal and medial area within stretch panels around the area of ??the board around the area of ??the external elastic vessel lumen area and calculate the neointimal area / medial area; immunohistochemistry assay vessel wall, MMP-2, Bax and Bcl-2 protein positive expression rate, TUNEL assay apoptosis rate. Results of the control group rat carotid artery only see a single layer of endothelial cells in the lumen side; experimental group after arterial injury 3d visible proliferation of VSMCs endovascular surface, 14d neointimal formation and further thickening, extracellular matrix also gradually increases. Injury NIA / MA, NIA / IEM increases gradually the 14d reached its maximum. Atorvastatin Atorvastatin calcium intervention groups, all with the experimental group were lower statistically significant. MMP-2, Bcl-2 and Bax protein expression levels of both little expression in normal vessel wall, but relatively low. Experimental group after 14 days of MMP-2 protein levels continued to rise in 28 days the expression levels than 14 days reduced; Bcl-2 protein expression levels have been maintained at high levels; the Bax protein postoperative began to increase, 7d gradually reduced. Atorvastatin Atorvastatin calcium can reduce the blood vessel damage, MMP-2, Bcl-2 protein expression, increased expression of Bax protein. TUNEL staining negative normal vessel wall; vascular injury TUNEL-positive cells first increased and then decreased. Atorvastatin calcium the apoptosis rate increase, its intensity and time. Conclusion Atorvastatin Atorvastatin calcium can significantly inhibit vascular injury intimal hyperplasia, and its role in the effectiveness and duration of action of the drug. The mechanism of the drug atorvastatin Atorvastatin calcium causes apoptosis-related protein expression changes that promote cell proliferation, Bcl-2, MMP-2 protein expression decreased, while regulating Bax protein expression, bax/bcl-2 increases, this may be one of its mechanisms.

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