PPARγ对高糖诱导THP-1巨噬细胞CD36表达及脂质蓄积的调节

Regulation of PPAR γ on the expression of CD36 and lipid accumulation induced by high glucose in THP-1 macrophages

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,10 mM 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<0.05)。结论提示高糖所诱导的CD36表达可能是由PPARγ所介导的。本实验的研究将对糖尿病性As病变的防治具有重要意义。

【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 CD36 mRNA, and CD36 protein were significantly suppressed（P 0.05） by GW9662, and it was observed by oil red O stain that the intracellular lipid droplets be remarkably reduced in THP-1 macrophages subsequently. 【Conclusions】It is suggested that PPAR γregulate the expression of CD36 and lipid accumulation induced by high glucose in THP-1 macrophages.