VLDL和ox-LDL对单核巨噬细胞的作用及机制探讨

The cooperation effects of VLDL and ox-LDL on monocyte-macrophage cell

目的:探讨极低密度脂蛋白(VLDL)、氧化修饰的低密度脂蛋白(ox-LDL)对单核巨噬细胞的作用及机制。方法:分析VLDL、ox—LDL对单核巨噬细胞清道夫受体A(SRA)、VLDL受体(VLDLR)基因转录、细胞因子肿瘤坏死因子(TNF—α)、基质金属蛋白酶(MMP-9)蛋白质表达,以及细胞生长状态的影响。结果:①VLDL增加ox-LDL介导的巨噬细胞SRA mRNA及蛋白质表达,ox—LDL则能增加VLDL介导的巨噬细胞VLDLR基因转录;②VLDL与ox—LDL协同作用显著减少巨噬细胞抗脂质摄取载脂蛋白E分泌;③两种脂蛋白能诱导巨噬细胞TNF-α及MMP-9释放,并能抑制巨噬细胞凋亡,促进增殖。结论:VLDL、ox-LDL对单核巨噬细胞增生、细胞因子释放及脂蛋白受体表达均有协同作用,可能体内的情况多为两种脂蛋白的协同作用。

Objective: To probe effects of VLDL and ox-LDL on foam cell induced by monocyte-macrophage. Methods:The roles of VLDL and ox-LDL in monocyte-macrophages scavenger receptor A(SRA) and very low density lipoprotein receptor (VLDLR) , mRNA expression .tumor necrosis factor-α(TNF-α)and matrix metallopro-teinase-9 (MMP-9) protein expression and cell growth state were analyzed. Results: VLDL increased ox-LDL induced macrophages SRA, mRNA and protein expression, ox-LDL augmented VLDL induced macrophages VLDLR, mRNA expression; VLDL combined with ox-LDL significantly inhibited macrophage-derived apoE secretion. These two lipoproteins induced proinflammatory cytokines TNF-α and MMP-9 release, and inhibited macrophages apoptosis and promoted cell proliferation. Conclusion:VLDL and ox-LDL may have many cooperation roles in monocyte-macrophage cell growth, cytokines release and lipoprotein receptor expression.