摘要
从高甘油三酯(HTG)大鼠动物模型中获取纯度较高、并有生物活性的高甘油三酯-极低密度脂蛋白(HTG-VLDL)。用乳过氧化物酶法^(121)Ⅰ标记HTG-VLDL,并将此^(125)Ⅰ-HTG-VLDL与正常大鼠腹腔巨噬细胞在体外共同培养,测得^(125)I-HTG-VLDL在该细胞的吸收,降解的时间曲线、剂量曲线及竞争抑制曲线。实验结果表明:^(125)Ⅰ-HTG-VLDL与鼠腹腔巨噬细胞的结合与降解具有时间饱和性、剂量饱和性及竞争抑制现象。提示鼠腹腔巨噬细胞表面可能存在能与HTG-VLDL结合并具受体性质的结合部位。HTG-VLDL可能通过受体途径的介导进入鼠腹腔巨噬细胞中代谢。
Pure and active hypertriglyceridemic very low density lipoprotein (HTG-VLDL) was obained from hypertriglyeeridemic rats. Laotoperoxidase was used for labelling rat HTG-VLDL with Na 125I. The 125I-HTG-VLDL was incubated with normal cultured rat peritoneal macrophagea in vitro the uptake and degradation time curves, dose curves, and competitive inhibition effect of the 125I-HTG-VLDL in macrophages were measured.Eesults showed that saturated uptake and degradation of 125I-HTG-VLDL increased with increasing concentrations of 125I-HTG-VLDL and incubation time. Competition experiments showed that increasing concentrations of radio-inert HTG-VLDL or normal-VLDL (n-VLDL) were effective in inhibiting the degrad-tion of macrophage 125I-HTG-VLDL.From the above results, we suggest that there may be specific binding sites with receptor characterization on rat peritoneal maorophages to recognize HTG-VLDL, and the metabolism of HTG-VLDL in macrophages may be mediated by these receptors.
出处
《上海医科大学学报》
CSCD
1990年第5期392-397,共6页
Journal of Fudan University(Medical Science)
关键词
甘油三酯
脂蛋白
腹腔
巨噬细胞
hypertriglyceridemic very low density lipoprotein
rat peritoneal macrophages
binding site
