Atorvastatin attenuates atherosclerosis of common carotid artery in apolipoprotein E gene-deficient mice by down-regulating NF-κB
10.3760/cma.j.issn.1673-4165.2015.08.008
- VernacularTitle:阿托伐他汀通过下调核因子-κB减轻载脂蛋白E基因缺陷小鼠颈总动脉粥样硬化
- Author:
Qinglin SUN
;
Mei WU
;
Xudong PAN
;
Aijun MA
;
Ting WANG
;
Xing XIAO
;
Lan WANG
- Publication Type:Journal Article
- Keywords:
Atherosclerosis;
Carotid Artery,Common;
Hydroxymethylglutaryl-CoA Reductase Inhibitors;
NF-κB;
Inflammation;
Disease Models,Animal;
Apolipoproteins E;
Mice;
Atorvastatin
- From:
International Journal of Cerebrovascular Diseases
2015;(8):611-616
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of atorvastatin on atherosclerosis formation of common carotid artery and its possible mechanism. Methods A total of 36 male apolipoprotein E gene knockout (ApoE-/-) mice were randomly divided into 3 groups: a control group, a model group, and an atorvastatin group. The mice of the control group were fed with normal diet and received a sham operation, while the mice in the model group and the atorvastatin group were given high fat diet and received a right common carotid artery cannulation. At 5 weeks after procedure, the mice in the model group and the atorvastatin group were intragastric administration of normal saline and atorvastatin (10 mg/kg daily), respectively. At 8 weeks after procedure, the blood from femoral arteries was obtained for biochemical detection, then right common carotid arteries were taken out for histopathological study. Real-time quantitative polymerase chain reaction (PCR) was used to detect the expression levels of NF-κB mRNA in the plaques. Western blotting was used to detect phosphorylated NF-κB p65. Results The lipid levels in the model group and the atorvastatin group were significant higher than those in the control group (al P<0. 05). The lipid level in the atorvastatin group was lower than that in the model group, but there was no significant difference (P> 0. 05 ). The histopathological study showed that the obvious plaque formation and the necrotic core and neovessels in plaques were observed in the model group; obviously thickened intima and more intact endothelial cel s in the vessel wal were observed in the atorvastatin group. The plaque burden in the model group and the atorvastatin group was significantly higher than that in the control group (al P<0. 001), while the plaque burden in the atorvastatin group was significantly less than that in the model group (P<0. 001). Real-time fluorescence quantitative PCR detection showed that the expression levels of NF-κB mRNA in the model group and the atorvastatin group were significantly higher than that in the control group (al P<0. 001), and the expression level of NF-κB mRNA in the atorvastatin group was significant lower than that in the model group (P= 0. 022). Western blotting showed that the expression level of the phosphorylated NF-κB p65 was significantly higher than that of the control group (P<0. 001), and the expression level of the phosphorylated NF-κB p65 was significantly lower than that in the model group (P<0. 001). Conclusions Atorvastatin may reduce atherosclerosis in the common carotid artery in ApoE-/-) mice by down-regulating NF-κB.
