中国动脉硬化杂志2012，Vol.20Issue(2)：121-124,4.
过氧化体增殖物激活型受体γ对巨噬细胞脂质蓄积及CD36表达的影响
Effect of Peroxisome Proliferator-Activated Receptor-γ on Cholesterol Accumulation and CD36 Expression in THP-1 Macrophages
摘要
Abstract
Aim To investigate the effects of peroxisome proliferator-activated receptor-"y ( PPAR-y) on cholesterol accumulation and CD36 expression in THP-1 macrophages.Methods Mononuclear cells were induced to differentiate into THP-1 macrophages by phorbol myristate acetate (160 nmol/L) co-incubation for 24 h. THP-1 macrophages were co-incubated with 50 mg/L oxidize low-density lipoprotein (ox-LDL) and PPAR*y agonist Ciglitazone( 10 (j,mol/L; C ) and PPAR-y antagonist GW9662(10 (junol/L;D)for 24 h, and the cells mixed with (B) and without (A) ox-LDL were as the control groups. Cellular total cholesterol was determined by high performance liquid chromatography analysis. CD36 mRNA and protein levels were determined by reverse transcription-polymerase chain reaction ( RT-PCR) and Western blot respectively. Results High performance liquid chromatography analysis demonstrated the amount of cellular total cholesterol were 76. 28 ± 10. 36( A) , 121. 63 ± 13. 32( B) , 136. 23 ± 14. 78( C) , 98. 52 ± 11. 45( D) mg per gram protein. PPAR-y antagonist GW9662 inhibited CD36 mRNA and protein synthesis. Ciglitazone increased CD36 mRNA and protein synthesis. The ratios of CD36/GAPDH were 0. 78( A) , 0.94(B), 1. 12(C), 0.52(D) respectively. Western blot re-suits conform to RT-PCR outcomes. Conclusion Antagonist of PPAR-y may decrease cholesterol accumulation anddownregulate ox-LDL-induced CD36 expression in THP-1 macrophages.关键词
THP-1巨噬细胞/CD36/过氧化体增殖物激活型受体γ/氧化型低密度脂蛋白/脂质蓄积Key words
THP-1 Mcrophage/Class B Scavenger Receptor CD36/Peroxisome Proliferator-Activated Recep-tor-"y/Oxidize Low-Density Lipoprotein/ Cholesterol Accumulation分类
医药卫生引用本文复制引用
曾颖,孙玉慧,黄延锦,易光辉..过氧化体增殖物激活型受体γ对巨噬细胞脂质蓄积及CD36表达的影响[J].中国动脉硬化杂志,2012,20(2):121-124,4.基金项目
湖南省教育厅重点基金项目(09A078) （09A078）
