[1]成小凤,刘小燕,宋凌鲲,等.阿托伐他汀钙调节PPARγ和NF-κB活性参与巨噬细胞泡沫化的形成[J].南方医科大学学报,2014,(06):896.
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阿托伐他汀钙调节PPARγ和NF-κB活性参与巨噬细胞泡沫化的形成()
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《南方医科大学学报》[ISSN:/CN:]

卷:
期数:
2014年06期
页码:
896
栏目:
出版日期:
2014-06-15

文章信息/Info

Title:
Atorvastatin inhibits macrophage-derived foam cell formation by suppressing the
activation of PPARγ and NF-κB pathway
作者:
成小凤刘小燕宋凌鲲何云李小庆张浩
关键词:
阿托伐他汀钙PPARγNF-κBTHP-1细胞细胞泡沫化
Keywords:
atorvastatin peroxisome proliferator-activated receptor γ nuclear factor-κB THP-1 cells macrophage-derivedfoam cells
摘要:
目的探讨阿托伐他汀钙是否通过调节PPARγ和NF-κB活性来抑制Ox-LDL诱导的THP-1巨噬细胞泡沫化形成。方法
THP-1巨噬细胞与10、20、40 μmol/L阿托伐他汀钙分别预孵育2 h,PBS洗2次,然后与60 μg/ml ox-LDL共孵育48 h后,通过酶
荧光法检测细胞胆固醇酯与总胆固醇比值,油红O染色观察细胞胞浆内脂质蓄积情况,Western blot 分析清道夫受体CD36、
SRA的表达,p-iκB和PPARγ的表达,以及ATP结合盒转运蛋白A1(ABCA1)的表达变化。用荧光探针DIL标记ox-LDL的方
法,观察阿托伐他汀钙对THP-1巨噬细胞结合ox-LDL能力的影响。结果阿托伐他汀钙浓度依赖性降低THP-1巨噬细胞脂质
蓄积和抑制清道夫受体CD36和SRA的表达,同时上调ABCA1表达,并减弱PPARγ和p-iκB活性(P<0.05)。荧光探针DIL标记
ox-LDL的方法显示阿托伐他汀钙浓度依赖性降低THP-1巨噬细胞结合ox-LDL能力(P<0.05)。结论阿托伐他汀钙抗动脉硬
化作用可能部分通过降低PPARγ和p-iκB活性来抑制脂质蓄积。
Abstract:
Objective To evaluate whether atorvastatin inhibits oxidized low-density lipoproteins (Ox-LDL)-stimulated foam
cell formation from THP-1 macrophages by regulating the activation of peroxisome proliferator-activated receptor γ (PPARγ)
and nuclear factor-κB (NF-κB). Methods THP-1 macrophages were pretreated with 10, 20, or 40 μmol/L atorvastatin for 2 h,
and after washing with PBS twice, the cells were incubated with 60 μg/ml of Ox-LDL for 48 h. The quantity of intracellular
lipid of the cells was detected with Oil red O staining and enzymatic fluorometric method. The expression of the scavenger
receptors of CD36 and SRA were analyzed with Western blotting. We also examined the effect of atorvastatin on adenosine
triphosphate (ATP)-binding cassette transporter A1 (ABCA1) expression and the activation of PPARγ and p-iκB, and further
assessed the capacity of the macrophages to bind to Dil-oxLDL. Results Atorvastatin potently inhibited ox-LDL-induced
macrophage-derived foam cell formation, down-regulated the expression of CD36 and SRA, and up-regulated the expression
of ABCA1. Atorvastatin markedly suppressed the activation of PPARγ and p-iκB in ox-LDL-stimulated THP-1 macrophages
(P<0.05) and significantly decreased the Dil-oxLDL-binding capacity of the macrophages (P<0.05). Conclusion Atorvastatin as
an effective anti-atherosclerosis agent can suppress the activation of PPARγ and p-iκB to reduce lipid accumulation in
macrophages.

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更新日期/Last Update: 1900-01-01