Scavenger Receptor Expression in Monocyte-macrophages and Accumulation of Oxidized LDL in Dialysis Patients

目的探讨透析患者动脉粥样硬化的发生机制。研究了血液透析患者和健康对照者单核-巨噬细胞中SR的表达，并制备了抗氧化LDL抗体，检测了4例血液透析患者和4例年龄和性别匹配的对照者中SR mRNA的表达。单核细胞被允许分化成巨噬细胞在体外培养7天，SR I型和II型mRNA的表达进行了分析与逆转录-聚合酶链反应和定量使用Southern印迹的辐射密度。只有SR I型表达在分化过程中增加，并在患者中加速1或2天，并在5天后增强，与对照组相比，通过使用抗氧化LDL抗体的ELISA方法，进行血液透析（HD）的尿毒症患者的血浆脂质过氧化反应。血浆氧化型低密度脂蛋白（oxidized LDL，OLDL）水平明显升高，分别为54.4 <plus-minus>± 12.5 μ g/ml和28.1 ± <plus-minus>8.4 μ g/ml。动脉硬化闭塞症（阿索）患者血浆氧化型低密度脂蛋白（oxidized LDL）和PCOH水平显著高于非阿索患者，总胆固醇、甘油三酯和LDL-脂蛋白水平在ASO患者与非ASO患者之间无显著差异。可能是通过I型的上调，这可能有助于这些患者中动脉粥样硬化的发展。

To elucidate the machanism of atherosclerosis in dialysis patients. SR expression was studied in monocyte-macrophages from dialysis patents and healthy controls, and anti-oxidized LDL antibody was developed.SR mRNA expression was examined in four hemodialysis patients and four controls matched for age and sex. Monocytes were allowed to differentiate into macrophages in in vitro cultures for seven days and SR type I and II mRNA expression were analyzed with the reverse transcription-polymerase chain reaction and quantitated using radiation densities of Southern blots. Only SR type I expression increased during differentiation and was accelerated by one or two days and enhanced after five days in patients, as compared to controlsPlasma lipid peroxidation in uremic patients undergoing hemodialysis (HD) by means of a ELISA method using anti-oxidized LDL antibody. Plasma oxidized LDL levels were significantly elevated 54.4<plus-minus>12.5mug/ml in the patients, while being 28.1<plus-minus>8.4mug/ml in normal controls. Plasma oxidized LDL and PCOOH levels of the subjects associated with arteriosclerosis obliterance (ASO) were significantly higher than that of patients without ASO.In the total cholesterol, trigyceride, and LDL-lipoprotein, there were no significant between the patients with and withoutIn conclusion, oxidized LDL SR expression is enhanced in macrophages from dialysis patients, probably by up-regulation of type I.which may contribute to the development of atherosclerosis in these patients.