单核巨噬细胞摄取极低密度脂蛋白机制的初步研究

目的：探讨单核巨噬细胞摄取极低密度脂蛋白（VLDL）的机制和途径。方法：观察单核巨噬细胞结合VLDL的活性、载脂蛋白E（apoE)配体活性及清道夫受体A（SRA）抗体的作用，分析VLDL对单核巨噬细胞SRAmRAN、蛋白质表达以及VLDL受体（VLDLR）基因转录的影响。结果：（1）单核巨噬细胞既能结合VLDL，又能结合缺乏apoE配体活性的VLDL（tryp-VLDL)，其总结合能力与2种脂蛋白浓度呈显著正相关（前者r1=0．71，后者r2＝0．63），但与结合VLDL能力相比，巨噬细胞结合tryp-VLDL的能力下降约50％；（2）SRA抗体对单核巨噬细胞结合^125I－VLDL活性无显著影响；（3）VLDL显著增加巨噬细胞VLDLR基因转录，而对巨噬细胞SRAmRNA及蛋白质表达作用不明显。结论：单核巨噬细胞可能通过apoE依赖（可能是VLDLR）或非依赖途径介导的VLDL摄取，SRA在此过程中不起重要作用。

The preliminary study on the machenism of uptaking of very low density lipoprotein by monocyte-macrophage cells

Objective The processes responsible for the uptake of very low density lipoprotein(VLDL) by monocyte macrophage cells were investigated. Methods The effects of VLDL concentration, apoE ligand activity and scavenger receptor A (SRA) on the binding of 125 I VLDL to monocyte macrophages were analysed. The influence of VLDL on SRA mRNA and protein expression and VLDL receptor gene translation was probed. Results (1) The differentiated monocyte macrophages induced 125 I VLDL uptake by dose dependent pathway( r =0 71, P <0 05), tryp treated VLDL (lack of apoE ligand activity) significantly decreased the cell associated binding (about 50%), but macrophages also could uptake tryp VLDL by dose dependent pathway( r =0 63, P <0 05); (2)SRA antibody had no effects on 125 I VLDL binding to macrophage cells; (3)VLDL could induce macrophage VLDL receptor(not SRA) mRNA expression. Conclusions Monocyte macrophages could directively intake VLDL by the apoE dependent (may be VLDL receptor) or apoE independent pathways, SRA may not be involved in VLDL uptake of monocyte macrophages .