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[炎症细胞因子与低密度脂蛋白(LDL)的过氧化]

[Inflammation cytokines and peroxidation of low density lipoproteins (LDL)].

作者信息

Mazière J C, Mazière C

机构信息

Laboratoire de Biochimie, CHRU d'Amiens, Hôpital Nord.

出版信息

C R Seances Soc Biol Fil. 1995;189(5):811-25.

PMID:8673628
Abstract

The effect of the inflammatory cytokins TNF-alpha, oncostatin M and interleukine 1 (IL1) on low density lipoprotein (LDL) oxidative modification have been studied on UNA endothelial cells or U937 monocytes in culture, by measuring the end products of lipid peroxydation (TBARS) and the relative electrophoretic mobility of the particle. TNF-alpha as well as oncostatin M stimulated in a dose-dependent manner the LDL peroxidation induced either by endothelial cells or U937 monocytes, and induced an increase in the uptake of modified LDL by J774 macrophages. Both TNF-alpha and oncostatin enhanced the superoxide anion production by endothelial cells or monocytes. In contrast, IL1 did not influence LDL cellular oxidation, but increased cholesterol esterification by stimulating the Acyl coenzyme A: cholesterol-0-acyltransferase (ACAT) activity of J774 macrophages. If IL1 acts on cholesteryl ester deposition by a mechanism differing from those of TNF-alpha or oncostatin M, all the studied cytokins may increase cholesteryl ester deposition. These results point at the potential promoting action of inflammatory processes in the progress of atherogenesis.

摘要

通过测量脂质过氧化的终产物(硫代巴比妥酸反应物,TBARS)以及颗粒的相对电泳迁移率,研究了炎性细胞因子肿瘤坏死因子-α(TNF-α)、制瘤素M和白细胞介素1(IL-1)对培养的UNA内皮细胞或U937单核细胞中低密度脂蛋白(LDL)氧化修饰的影响。TNF-α以及制瘤素M以剂量依赖的方式刺激内皮细胞或U937单核细胞诱导的LDL过氧化,并导致J774巨噬细胞对修饰LDL的摄取增加。TNF-α和制瘤素M均增强了内皮细胞或单核细胞的超氧阴离子产生。相比之下,IL-1不影响LDL的细胞氧化,但通过刺激J774巨噬细胞的酰基辅酶A:胆固醇-O-酰基转移酶(ACAT)活性增加胆固醇酯化。如果IL-1通过不同于TNF-α或制瘤素M的机制作用于胆固醇酯沉积,那么所有研究的细胞因子可能都会增加胆固醇酯沉积。这些结果表明炎症过程在动脉粥样硬化进展中具有潜在的促进作用。

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