Atorvastatin inhibits macrophage- derived foam cell formation by suppressing the activation of PPARγand NF-κB pathway
10.3969/j.issn.1673-4254.2014.06.28
- VernacularTitle: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
- Author:
Xiaofeng CHENG
1
;
Xiaoyan LIU
;
Lingkun SONG
;
Yun HE
;
Xiaoqing LI
;
Hao ZHANG
Author Information
1. 第三军医大学新桥医院心血管内科
- Keywords:
atorvastatin;
peroxisome proliferator-activated receptor γ;
nuclear factor-κB;
THP-1 cells;
macrophage-derived foam cells
- From:
Journal of Southern Medical University
2014;(6):896-900
- CountryChina
- Language:Chinese
-
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 receptorγ(PPARγ) and nuclear factor-κB (NF-κB). Methods THP-1 macrophages were pretreated with 10, 20, or 40μmol/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 PPARγand 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 PPARγand 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.
