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血清对人单核细胞衍生巨噬细胞低密度脂蛋白代谢的影响。

The effect of serum on low density lipoprotein metabolism of human monocyte-derived macrophages.

作者信息

Kotake H, Oikawa S, Naito T, Hayasaka K, Toyota T

机构信息

Third Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.

出版信息

Tohoku J Exp Med. 1993 Dec;171(4):285-95. doi: 10.1620/tjem.171.285.

Abstract

Macrophages oxidatively modify low density lipoprotein (LDL). These cells then recognize and take up oxidized LDL (OxLDL) via the scavenger receptor. In the present study, we examined the effect of lipoprotein depleted serum (LPDS) on the oxidative modification of LDL and its uptake and degradation by human monocyte-derived macrophages. LPDS inhibited LDL oxidation in a concentration-dependent manner and the complete inhibition was observed in the concentration from 2.5 to 10.0%. In the presence of 5% of LPDS, cell-associated 125I-LDL was reduced by 70%, compared with that in the absence of LPDS. In contrast, 125I-LDL degradation increased in the presence of LPDS. The ratio of degradation products to cell-associated radioactivity in the presence of LPDS was five-fold greater than that in the absence of LPDS. In the presence of LPDS, unlabeled LDL competed for about 50% of cellular uptake and degradation of 125I-LDL. In the absence of LPDS, however, unlabeled LDL competed for only 20% of uptake and only 30% of degradation of 125I-LDL. Unlabeled OxLDL competed for about 80% of uptake and degradation in the absence of LPDS. These results suggest that LPDS inhibited the production of OxLDL which was taken up by macrophages via the pathway for the OxLDL.

摘要

巨噬细胞可对低密度脂蛋白(LDL)进行氧化修饰。这些细胞随后通过清道夫受体识别并摄取氧化型LDL(OxLDL)。在本研究中,我们检测了脂蛋白缺乏血清(LPDS)对LDL氧化修饰及其被人单核细胞衍生巨噬细胞摄取和降解的影响。LPDS以浓度依赖的方式抑制LDL氧化,在2.5%至10.0%的浓度范围内观察到完全抑制。在存在5%LPDS的情况下,与不存在LPDS时相比,细胞相关的125I-LDL减少了70%。相反,在存在LPDS的情况下,125I-LDL的降解增加。存在LPDS时降解产物与细胞相关放射性的比率比不存在LPDS时高五倍。在存在LPDS的情况下,未标记的LDL竞争约50%的125I-LDL细胞摄取和降解。然而,在不存在LPDS的情况下,未标记的LDL仅竞争20%的摄取和30%的125I-LDL降解。在不存在LPDS的情况下,未标记的OxLDL竞争约80%的摄取和降解。这些结果表明,LPDS抑制了通过OxLDL途径被巨噬细胞摄取的OxLDL的产生。

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