地拉卓对人类单核细胞株源性巨噬细胞摄取乙酰化低密度脂蛋白的影响

Dilazep influence acetylated low density lipoprotein uptake through down-regulation of scavenger receptor expression in THP-1 derived macrophages

目的观察地拉卓(血管扩张及抗血小板药)对人类单核细胞株(THP-1)源性巨噬细胞摄取乙酰化低密度脂蛋白(Ac-LDL)的影响。方法以不加入地拉卓为对照组,以分别加入50、100μmol·L-1地拉卓为实验组;用细胞摄取Ac-LDL及Northern印迹方法,观察地拉卓对THP-1源性巨噬细胞受体摄取Ac-LDL以及对巨噬细胞清道夫受体-A mRNA表达的影响。结果与对照组比较,巨噬细胞对Ac-LDL结合量和降解量随地拉卓浓度的增加而被明显抑制(均P<0.01);巨噬细胞ScR-AmRNA表达随地拉卓浓度的增加而减弱。结论地拉卓抑制THP-1源性巨噬细胞对Ac-LDL结合和降解的作用是通过抑制ScR-A mRNA的表达来实现,其对动脉粥样硬化形成早期可能具有抑制作用。

Objective To clarify whether dilazep can influence uptake （including binding and degradation） of acetylated low density lipoprotein （ Ac - LDL ） by THP - 1 derived macrophage and its macrophage scavenger receptor class A type Ⅰ and type Ⅱ （ ScR - A ） expression. Methods Macrophages differentiated from THP- 1 monocytes by treatment of 12 - O - tetradecanoylphobol - 13 - acetate. Macrophages incubated with different concentration of dilazep, then their uptake （ including 4 ℃ binding and 37 ℃ degradation ） of Ac - LDL and ScR - A mRNA expression were measured. Results Pretreatment of 50 and 100 μmol · L^-1 of dilazep, significantly decreased Ac - LDL binding and degradation with dilazep concentration - dependent manner. The macrophage ScR - A mRNA expression was markedly attenuated by treatment of 50 μmol · L^-1 dilazep and almost completely abolish by treatment of 100 μmol · L^-1 dilazep. Conclusion Dilazep could inhibit Ac -LDL uptake through attenuate macrophage ScR - A expression in THP - 1 derived macrophages. These results suggest that dilazep may have preventive effect on early stage of atherogenesis.