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肿瘤坏死因子增强单核细胞和内皮细胞对低密度脂蛋白的氧化修饰。

Tumor necrosis factor enhances low density lipoprotein oxidative modification by monocytes and endothelial cells.

作者信息

Maziere C, Auclair M, Maziere J C

机构信息

Laboratoire de Biochimie, Faculté de Médecine Saint-Antoine, Paris, France.

出版信息

FEBS Lett. 1994 Jan 24;338(1):43-6. doi: 10.1016/0014-5793(94)80113-4.

Abstract

The effect of tumor necrosis factor on the oxidative modification of LDL by U937 human monocytes or murine endothelial cells was studied by determination of the lipid peroxidation product content and the electrophoretic mobility of the particle. In the range of concentrations from 2.5 to 10 ng/ml, the cytokine induced a dose-dependent increase in cellular-induced oxidation of LDL. This effect was accompanied by a stimulation of LDL degradation by J774 macrophage-like cells. Concurrently, the TNF-treated cells secreted superoxide anion with a higher rate. Since LDL oxidation is believed to be an important feature in the formation of the atherosclerotic plaque, the described effects of TNF might be of importance in long-term exposure to this cytokine during inflammation.

摘要

通过测定脂质过氧化产物含量和颗粒的电泳迁移率,研究了肿瘤坏死因子对U937人单核细胞或小鼠内皮细胞氧化修饰低密度脂蛋白(LDL)的影响。在2.5至10 ng/ml的浓度范围内,该细胞因子诱导细胞诱导的LDL氧化呈剂量依赖性增加。这种效应伴随着J774巨噬细胞样细胞对LDL降解的刺激。同时,经TNF处理的细胞以更高的速率分泌超氧阴离子。由于LDL氧化被认为是动脉粥样硬化斑块形成的一个重要特征,TNF的上述作用在炎症期间长期暴露于这种细胞因子时可能具有重要意义。

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