摘要
目的观察高糖对HDL调节THP-1巨噬细胞清道夫受体CD36和过氧化体增殖物激活型受体γ(PPARγ)表达的影响。方法用50 mg/L ox-LDL、50 mg/L ox-LDL+50 mg/L HDL、50 mg/L ox-LDL+50 mg/L HDL+20 mmol/L D-葡萄糖、50 mg/L HDL、50 mg/L HDL+20 mmol/L D-葡萄糖孵育THP-1巨噬细胞24 h,采用油红O染色观察细胞内脂质蓄积情况,RT-PCR和Western Blot分别检测CD36、PPARγ、p-PPARγmRNA和蛋白的表达。结果加用HDL组明显减少脂质蓄积,加用HDL组的CD36 mRNA和蛋白的表达下调,PPARγ的mRNA和蛋白及p-PPARγ的蛋白表达上调;而同时加用50 mg/L HDL和20 mmol/L葡萄糖组CD36和PPARγ的mRNA及蛋白表达上调,而p-PPARγ的表达下调(P<0.05),并促进脂质蓄积。结论高糖可使HDL抑制CD36表达及脂质蓄积的作用减弱。
Aim To investigate the effect of high glucose on the expression of CD36 and peroxisome proliferator- activated receptor gamma (PPAR3,) regulated by high density lipoprotein (HDL) in THP-1 macrophage. Methods THP-1 macrophages were incubated with 50 mg/L ox-LDL, 50 mg/L ox-LDL +50 mg/L HDL, 50 mg/L ox-LDL +50 mg/ L HDL + 20 mmol/L D-Glucose, 50 mg/L HDL, 50 mg/L HDL + 20 mmol/L D-Glucose for 24 h. The lipid accumula- tion was detected by oil red 0 stain. CD36 and PPARγ/mRNA were determined by reverse transcription-polymerase chain reaction ( RT-PCR), respectively. CD36, PPARγ and p-PPARγ/protein was determined by Western Blot. Results The expression of CD36 mRNA and protein was significantly suppressed (P 〈 0.05) by HDL, which significantly reduced the lipid accumulation. In the 50 mg/L HDL and 20 mmol/L glucose groups, the mRNA and protein of CD36 and PPARs,, and the lipid accumulation were signifcantly increased ( P 〈 0.05 ). However, the expression of p-PPAR,/was markedly reduced (P 〈 0.05). Conclusion The data indicated that high glucose can weaken the role of HDL in sup- pressing CD36 expression and lipid accumulation.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2014年第6期553-557,共5页
Chinese Journal of Arteriosclerosis
基金
国家自然科学基金资助项目(81270360)
湖南省科技厅科技计划重点项目(2014FJ2012)
湖南省卫生厅医药卫生科研计划课题项目(B2014-070)