期刊论文

中文

中国现代医学杂志

1005-8982

2014

24

30

18-23

国家自然科学基金资助项目（No:81270360）； 湖南省科技厅科技计划重点项目（No:2014FJ2012）； 湖南省卫生厅医药卫生科研计划课题项目（No:B2014-070）；

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目的观察PPARγ 对高糖诱导THP-1巨噬细胞CD36表达及脂质蓄积的调节。方法联合或单独使用50 mg/L Ox-LDL,20 mM D-葡萄糖,10mM GW9662孵育THP-1巨噬细胞24 h。采用逆转录-聚合酶链式反应(RT-PCR)检测CD36、PPARγmRNA的表达;采用Western印迹法检测CD36蛋白质;用油红 O 染色观测细胞内脂质蓄积情况。结果PPARγ 拮抗剂(GW9662)明显地抑制了高糖所诱导的脂质蓄积及 CD36的表达,油红O染色可见细胞内脂滴明显地减少。CD36、PPARγmRNA,CD36蛋白质的表达明显下降(P

【Objective】To investigate the effect of PPAR γ on the expression of CD36 and the Lipid Accumulation induced by High Glucose in THP-1 Macrophages. 【Methods】THP-1 macrophages were incubated for 24 h with 50 mg/L Ox-LDL, 20 mM D-glucose, 10 mM GW9662, combined or respectively. The lipid accumulation was detected by oil red O stain. CD36 and PPARγ mRNA level were determined by reverse transcription-polymerase chain reaction（RT-PCR）, respectively. CD36 protein level was determined by Western blotting.【Results】The expression of PPAR γ and ...