| Objective:To preliminarily investigate the influence of Rosuvastatin on the neointimal hyperplasia and its mechanism in rat carotid arteries after balloon injury.Methods:48 male SD rats were randomly and equally divided into Rosuvastatin group,the injured group and control group,and the latter two groups shared 24 rats.Each rat was subjected to balloon injury on the left common carotid artery,and control artery without injury was on the right artery.Rosuvastatin group rats were given Rosuvastatin(dissolved in Nacl,gavage) at 5 mg /(kg·d) 3 days before injury until sacrificed,while the injured group rats were given vehicle instead.All rats were sacrificed on 7 d or 14 d after injury,and the common carotid arteries were harvested for HE staining and TUNEL apoptosis analysis.Meanwhile,SMα-actin,PCNA, PTEN and phosphor-PTEN(p-PTEN) were detected by immunohistochemistry,and the changes of PTEN and p-PTEN expression were measured by Western-blot.Results:(1) The area of neointimal and the area ratio of neointimal to media decreased significantly in 14 d in Rosuvastatin group,with 26%increase in luminal area(compared with 14 d in injured group,P＜0.05).(2) Lower positive cell rate of PCNA,(15.6±2.1)%),and higher positive cell rate of TUNEL,(26.8±2.7)%,were observed in 14 d in Rosuvastatin group than in 14 d in injured group(P＜0.05).(3) It was shown that PTEN and p-PTEN were found mainly in the cytoplasma of neointimal vascular smooth muscel cells(VSMCs).(4) The ratio of p-PTEN to total PTEN were attenuated in both 7 d and 14 d in Rosuvastatin group(compared with the injured group respectively,P＜0.05).Conlusion:(1) Rosuvasatin could inhibit neointimal hyperplasia and restenosis after balloon injury.(2) Rosuvastatin could induce apoptosis and inhibit proliferation in VSMCs.(3) Rosuvastatin could reduce the ratio of p-PTEN to total PTEN in rats injured carotid arteries.(4) These findings preliminarily suggested that Rosuvasatin could inhibit neointimal hyperplasia and restenosis through induction of apoptosis and inhibition of proliferation in VSMCs,which might be related to the expression of more active PTEN and less inactive p-PTEN. |
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