中文摘要：

在动脉粥样硬化发展的关键事件是由巨噬细胞和在 subendothelial 的泡沫房间的形成的类脂化合物举起动脉的空间。除由 scavenger 的修改低密度的脂蛋白(LDL ) 的举起以外调停受体的 endocytosis，巨噬细胞拥有组成的 macropinocytosis，它能够收起溶质的大数量。巨噬细胞泡沫房间形成能被在文化媒介增加浆液集中在 RAW264.7 房间导致。浆液导致的泡沫房间形成能被 phosphoinositide 3-kinase 禁止者， LY294002 或 wortmannin 堵住，它禁止了 macropinocytosis 然而并非调停受体的 endocytosis。进一步的分析显示 macropinocytosis 发生在充实 gangliosides 的膜区域。由没有影响 scavenger 的 -methylcyclodextrin-blocked macropinocytosis 的胆固醇弄空修改 LDL 的调停受体的 endocytosis。这些结果建议 macropinocytosis 可能是为在巨噬细胞的类脂化合物举起的重要机制之一。并且它做了重要贡献到类脂化合物累积和泡沫房间形成。

英文摘要：

The key event in the atherosclerosis development is the lipids uptake by macrophage and the formation of foam cell in subendothelial arterial space. Besides the uptake of modified low-density lipoprotein （LDL） by scavenger receptor-mediated endocytosis, macrophages possess constitutive macropinocytosis, which is capable of taking up a large quantity of solute. Macrophage foam cell formation could be induced in RAW264.7 cells by increasing the serum concentration in the culture medium. Foam cell formation induced by serum could be blocked by phosphoinositide 3-kinase inhibitor, LY294002 or wortmannin, which inhibited macropinocytosis but not receptor-mediated endocytosis. Further analysis indicated that macropinocytosis took place at the gangliosides-enriched membrane area. Cholesterol depletion by β-methylcyclodextrin-blocked macropinocytosis without affecting scavenger receptormediated endocytosis of modified LDLs. These results suggested that macropinocytosis might be one of the important mechanisms for lipid uptake in macrophage. And it made significant contribution to the lipid accumulation and foam cell formation.