摘要
目的观察过氧化体增殖物激活型受体1（PPARγ）反义寡核苷酸对THP-1巨噬细胞CD36表达及细胞胆固醇流入的影响，探讨PPAR7的作用及机制。方法用50mg／L氧化型低密度脂蛋白（OX—LDL）分别与不同浓度PPARγ的反义寡核苷酸（400nmol／L）、错义寡核苷酸（400nmol／L）或15μmol／LPPARγ激动剂ciglita-zone共同孵育THP—l巨噬细胞24h后，采用逆转录-聚合酶链反应和Western印迹分析分别检测CD36的表达，采用液体闪烁计数法检测[3H]胆固醇流入。，结果与OX—LDL组比较，PPARγ反义寡核苷酸下调巨噬细胞CD36的表达，且细胞胆固醇流入率下降（OX—LDL组为28．1％、反义寡核苷酸组为22．5％）。而ciglitazone则使巨噬细胞CD36的表达上调，胆固醇流入率明显增加（36．8％）。结论抑制PPARγ表达，可抑制THP-1巨噬细胞CD36的表达，并减少细胞胆固醇流入。
Objective To investigate the effect of peroxisome proliferator-activated receptor-γ （PPARγ） on CD36 expression and cholesterol influx in THP-1 macrophage. Methods After exposure of the cultured THP-1 macrophage to antisense PPAR3, oligonucleotide and ciglitazone for 24 hours, [ 3H] labeled Cholesterol influx was determined by FJ-2107P type liquid scintillator. CD36 mRNA and protein level were determined by reverse transcription-polymerase chain reaction （RT-PCR） and Western blotting respectively. Results Antisense PPARγ oligonucleotide inhibited CD36 expression and cholesterol influx in THP-1 macrophage. PPARγ agonist, ciglitazone, elevated CD36 in both protein and mRNA levels, and increased cholesterol influx in THP-1 macrophage. Conclusion Our results indicated that PPARγ may play an important role in CD36 expression and cholesterol influx in THP-1 macrophage.
出处
《中南医学科学杂志》
CAS
2011年第5期493-496,共4页
Medical Science Journal of Central South China
基金
湖南省教育厅科研项目(10C1165)
