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共轭亚油酸异构体可能会减少人类巨噬细胞黏附在内皮表面。

Conjugated linoleic acid isomers may diminish human macrophages adhesion to endothelial surface.

机构信息

Department of Biochemistry and Human Nutrition, Pomeranian Medical University, Szczecin, Poland.

出版信息

Int J Food Sci Nutr. 2012 Feb;63(1):30-5. doi: 10.3109/09637486.2011.593505. Epub 2011 Jul 1.

Abstract

Dysfunction of endothelial cells and activation of monocytes in the vascular wall are important pathogenetic factors of atherosclerosis. Conjugated linoleic acids (CLAs) can modulate the function of immune system in humans: reduce the concentration of atherogenic lipoproteins, and the intensity of inflammatory processes in the plasma. In this paper, we focus on macrophage's surface integrins (β1 integrin CD49d/CD29-(VLA4); Mac-1 as well as endothelial human vein endothelial cell (HUVEC) surface adhesins: vascular cell adhesion molecule-1 (VCAM-1) and intracellular cell adhesion molecule-1 (ICAM-1)) expression in relation to CLA isomer used during cell culture. Both CLA isomers decreased expression of VLA-4 and Mac-1 on macrophages compared with control cells (cultured with bovine serum albumine (BSA) or oxidized form of low-density lipoproteins). cis-9, trans-11 CLA isomer reduced ICAM-1 and VCAM-1 expression on the endothelium surface. Strong tendency to reduce of adhesion of macrophages to HUVEC in the cells cultured with CLA isomers was observed. The potential role of cis-9, trans-11 CLA in the reduction of adhesion of macrophages to the HUVEC--one of the important steps in the inflammatory process, can be considerate. These mechanisms may contribute to the potent anti-atherosclerotic effects of CLA in vivo.

摘要

内皮细胞功能障碍和血管壁中单核细胞的激活是动脉粥样硬化的重要发病因素。共轭亚油酸(CLA)可以调节人体免疫系统的功能:降低致动脉粥样硬化脂蛋白的浓度,以及降低血浆中炎症过程的强度。在本文中,我们专注于巨噬细胞表面整合素(β1 整合素 CD49d/CD29-(VLA4);Mac-1 以及内皮人静脉内皮细胞(HUVEC)表面黏附分子:血管细胞黏附分子-1(VCAM-1)和细胞间黏附分子-1(ICAM-1))的表达与细胞培养中使用的 CLA 异构体有关。与对照细胞(用牛血清白蛋白(BSA)或氧化型低密度脂蛋白培养)相比,两种 CLA 异构体均降低了巨噬细胞上 VLA-4 和 Mac-1 的表达。顺式-9,反式-11 CLA 异构体降低了内皮细胞表面的 ICAM-1 和 VCAM-1 的表达。在培养有 CLA 异构体的细胞中,观察到巨噬细胞与 HUVEC 黏附的强烈趋势降低。顺式-9,反式-11 CLA 减少巨噬细胞与 HUVEC 黏附的潜在作用——这是炎症过程中的重要步骤之一,可以考虑。这些机制可能有助于 CLA 在体内的强大抗动脉粥样硬化作用。

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