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氧化型低密度脂蛋白对小鼠腹腔巨噬细胞应激蛋白的诱导作用

Induction of stress proteins in mouse peritoneal macrophages by oxidized low-density lipoprotein.

作者信息

Yamaguchi M, Sato H, Bannai S

机构信息

Department of Biochemistry, Tsukuba University Medical School, Ibaraki, Japan.

出版信息

Biochem Biophys Res Commun. 1993 Jun 30;193(3):1198-201. doi: 10.1006/bbrc.1993.1752.

Abstract

The synthesis of 23-kDa and 34-kDa proteins in mouse peritoneal macrophages was enhanced when they were incubated with oxidatively modified low-density lipoprotein (LDL). This response required the oxidation of the lipid of the LDL, because native LDL had little effect and acetylated LDL enhanced the synthesis of 34-kDa protein only slightly. Since macrophages can bind and sequester oxidized LDL, they are subjected to an oxidative stress. The results suggest that the 34-kDa protein, which is identical with heme oxygenase, and the 23-kDa protein serve as stress protein that might afford protection against the oxidative stress.

摘要

当小鼠腹腔巨噬细胞与氧化修饰的低密度脂蛋白(LDL)一起孵育时,其23 kDa和34 kDa蛋白质的合成增强。这种反应需要LDL脂质的氧化,因为天然LDL几乎没有作用,而乙酰化LDL仅略微增强34 kDa蛋白质的合成。由于巨噬细胞可以结合并隔离氧化LDL,它们会受到氧化应激。结果表明,与血红素加氧酶相同的34 kDa蛋白质和23 kDa蛋白质作为应激蛋白,可能提供针对氧化应激的保护作用。

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