巨噬细胞集落刺激因子对小鼠腹腔巨噬细胞清道夫受体途径和细胞内胆固醇酯积聚的影响  

The Effect of Macrophage Colony-Stimulating Factor on Scavenger Receptor passway of Mouse Peritoneal-Macrophage and Cellular Cholesteryl Ester Accumulation

作　　者：陈兵[1] 范乐明[2] 蔡海江[2] 王南[2] 朱宇[2] 

机构地区：[1]南京鼓楼医院内科,南京210008 [2]南京医科大学动脉粥样硬化研究中心,南京210029

出　　处：《中国动脉硬化杂志》1997年第1期10-14,共5页Chinese Journal of Arteriosclerosis

摘　　要：为探索巨噬细胞集落刺激因子、清道夫受体、氧化型低密度脂蛋白与动脉粥样硬化的关系，观察了重组人巨噬细胞集落刺激因子对小鼠腹腔巨噬细胞清道夫受体途径的影响以及重组人巨噬细胞集落刺激因子对氧化型低密度脂蛋白所致细胞内胆固醇酯积聚的影响．结果发现重组人巨噬细胞集落刺激因子能增加培养的小鼠腹腔巨噬细胞表面的清道夫受体数目，使之对氧化型低密度脂蛋白的结合和降解呈现剂量和时间依赖性增加，并使细胞内胆固醇酯积聚增多．表明巨噬细胞集落刺激因子可通过增加清道夫受体数目使小鼠腹腔巨噬细胞对氧化型低密度脂蛋白的结合和降解增多，从而增加细胞内胆固醇酯含量，促进动脉壁内泡沫细胞形成．Aim The search for the relation between macrphage colony-stimulating factor (MCSF), scav- enger receptor (SR), oxidative modified low density lipoprotein (OLDL) and atherosclerosis (As). We studied the effect of recombinant human MCSF (rhM- CSF) on the SR passway of mouse peritoneal macrophage (MPM) and the effect of rhMCSF on cel-lular cholesteryl ester (CE) accumulation caused by OLDL.Methods Mouse peritoneal macrophages (MPM) were collected by routine method. LDL was isolated by density gradient ultracentrifugation, oxidized by CuCl2 and labeled either with 3, 3-dioctadecyl indocar- bocyamine (Dil) or with 125 I. The binding of DiI- OLDL and degradation of 125 I-OLDL by MPM and the intracellular content of CE were measured according to the methods of Stephen, Gold stein and Heider respec- tively.Results Recombinant human MSCF could increase the number of SR on cultured MPMs and enhance the binding and degradation of OLDL with a dose-and time-dependent mode. The cellular CE accumulation caused by OLDL was also enhanced by addition of rhMCSF.Conclusions MCSF may enhance the cellular binding and degradation of OLDL by increasing the number of SR on MPMs, hence increase the cellular CE content and promote the formation of foam cells in the vascular wall.

关 键 词：巨噬细胞 集落刺激因子 动脉粥样硬化 胆固醇酯 

分 类 号：R543.502[医药卫生—心血管疾病]