脂质转运和脂酶水解对低密度脂蛋白的修饰作用

Modify Low Density Lipoprotein by Lipid Transfer Activity and Triglyceride Hydrolysis

采用胆固醇脂转运蛋白（CETP）介导极低密度脂蛋白（VLDL）中甘油三酯（TG）与低密度脂蛋白（LDL）中胆固醇（CH）交换：再行脂蛋白脂酶（LPL）水解LDL中TG，对LDL进行修饰，引起LDL颗粒组成和大小的变化，探讨体内小而致密的LDL形成的可能途径，及易于致动脉粥样硬化（As）作用的机制。结果示CETP介导的脂质转运使LDL中TG含量增加，CH降低，颗粒直径轻微变大；再经LPL水解的共同作用，LDL中TG含量降低，颗粒变小。同时LDL中载脂蛋白B（apoB）免疫反应性也发生相应的变化，LDL中TG含量同apoB免疫反应性高度负相关。认为大而轻的A型LDL经修饰作用可转变为小而致密的B型LDL，富含TG的LDL不易于通过apoB受体途径清除，史易于氧化。

To study the probable way of the large. light lower density lipoprotein (LDL) changing into thelittle. dense LDL and the reason that pattern B LDL is more risk factor for atherosclerosis, LDLwere modified in vitro, which induced alterations in the size and lipid composition of LDL particles.Through exchang of cholesteryl in LDL with triglyceride in very low density lipoprotein (VLDL)mediated by cholesteryl ester transfer protein (CETP) and triglyceride hydrolysis, we found thattriglyceride content and the size of LDL particles increased significantly by the transformation ofCETP, the immunoreactivity of apolipoprotein B (apoB) was decreased (P<0.05). Subsequently,the hydrolysis of lipoprotein lipase (LPL) reduced the content oftriglyceride and the particle size, butimmunoreactivity ofapo B was increased. The content of triglyceride in LDL is negatively related withthe immunoreactivity of apoB was increased. The results indicate that modifying triglyceriderich LDLcan transform typical large-sized LDL pattern A into typical small-sized LDL pattern B, the latter isnot easy to be deleted by apoB receptor in vivo, and is easy to be oxidated, so LDL pattern B paysmore role in development of atherosclerosis.