Atorvastatin Calcium On The Rat Carotid Artery Intimal Hyperplasia After Balloon Injury And The Expression Of MMP-2

ObjectiveTo explore the pathogenesis of vascular stenosis, we have established rat carotid artery injury in animal models, we were observed at different time points VSMCs proliferation and vascular remodeling and to study atorvastatin calcium on the vascular endothelial injury induced proliferation of VSMCs inhibition and expression in vivo rat MMP-2,Bax,Bcl-2 and other apoptosis-related protein.MethodsSD rats to establish an animal model of carotid injury, animals were randomly divided into: sham-injured group, injured group and injured + atorvastatin calcium in the treatment group. Under the microscope by HE staining deteced 3,7,14,28 d vascular morphological changes, computer image analysis system detected neointimal thickness, internal elastic laminae around the area, external elastic plate around the area, lumen area of each group and calculate the neointimal area/medial area, stenosis index; detected by immunohistochemistry injury group and intervention group vascular wall cells MMP-2, Bax and Bcl-2 protein expression, TUNEL Detection of cell apoptosis. ResultsControl group, only to see the total intimal endothelial cell monolayer; the experimental group, after injury visible on the surface 3d endovascular proliferation VSMCs, 14d and the thickness of neointima formation, while also increasing the extracellular matrix. 14d medial area was significantly greater than when no damage blood vessels. 14d significantly less than the undama- ged side of the future. Injured 3-7 d, NIA / MA, NIA / IEM to 14 d of maximum. Atorvastatin treatment group compared with the experimental indexes have the opposite trend.Control group, cells in the vessel wall MMP-2, Bcl-2 and Bax protein level is relatively low. The experimental group MMP-2 protein levels continued to rise after 14 days, 28 days in the expression levels found on day 14 decreased; Bcl-2 protein levels have been increased; Bax protein also increased after surgery, 7d after decline. Atorvastatin calcium intervention group MMP-2, Bcl-2 protein levels compared with the experimental group decreased, but Bax protein increased compared with the experimental group.No TUNEL positive cells in sham-injured group;TUNEL positive cells after balloon injury in the first increased. Atorvastatin calcium increased the apoptosis rate, its role to strengthen with time.ConclusionsAtorvastatin calcium can inhibit intimal hyperplasia after vascular injury, its role and effectiveness of the role of time-related drugs. The role of mechanism of drug atorvastatin calcium leads to apoptosis-related protein expression changes that promote cell proliferation of Bcl-2, MMP-2 protein expression decreased, while Bax protein in regulating expression, bax/bcl-2 increases, which may be one of the mechanisms.