Study On Atorvastatin’s Attenuating Atherosclerosis Of Common Carotid Artery In Apolipoprotein E Gene-deficient Mice By Down-regulating NF-κB

Objective: To detect the expression of NF-κB in order to investigate the anti-atherosclerotic and anti-inflammatory effects of atorvastatin.Methods: Thirty-six male Apo E-/- mice were randomly divided into 3 groups: control group, model group and statin group. Mice of the control group were received a sham operation. While the mice of the model group and the statin group were given an operation with perivascular collar placement on the right common carotid artery to establish an AS model. From the 5th week after surgery, mice in statin group were intervened with atorvastatin(10 mg/kg/d per gavage), while mice in model group were given normal saline in stead. The serum samples were obtained via the femoral artery transection and the lipid levels of all mice were detected at the end of the 8th weeks after operation. Serial paraffin sections were routinely stained with hematoxylin and eosin to observe atherosclerotic lesion in the right common carotid artery. The m RNA level of NF-κB was quantified by real-time fluorescence quantitative RT-PCR(q RT-PCR).The expression level of NF-κB p65 was detected by western blotting.Results: The lipid levels from mice of model group and statin group were significant higher than those of control group(P<0.05). The lipid levels of the statin group were lower than those of the model group, but such difference was not statistical(P>0.05). The histopathological observation showed that there were evident lesions in model group, in which necrotic core and angiogenesis were noticed. The carotid intima of the statin group were thickened significantly. Relatively integrated endothelia cells could be found. The plaque burden of the model group and the statin group were significantly higher than that of the control group(both P<0.01), while the plaque burden was obviously reduced in statin group when compared with that of the model group(P<0.01). The NF-κB gene expression was higher in either model group or statin group compared with the control(both P<0.01).Compared with model group, the expression of NF-κB was decreased in statin group(P<0.05).The expression of phosphorylation of NF-κB p65 was much higher in model group than that in the control group(P<0.01). While it was obviously decreased in statin group when compared with that of the model group(P<0.01).Conclusions: Atorvastatin suppresses NF-κB activity in the AS plaque, suggesting the anti-atherosclerotic and anti-inflammatory effects of atorvastatin.