体内炎症不会损害abca1介导的高密度脂蛋白胆固醇外排能力。

Cholesterol Pub Date : 2012-01-01 DOI:10.1155/2012/610741
Remco Franssen, Alinda W M Schimmel, Sander I van Leuven, Simone C S Wolfkamp, Erik S G Stroes, Geesje M Dallinga-Thie
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引用次数: 11

摘要

HDL通过促进血管壁中脂质巨噬细胞的胆固醇外排提供动脉粥样硬化保护。体外研究表明炎症改变后HDL外排能力受损。我们评估了急性严重脓毒症和轻度慢性炎症性疾病对HDL外排能力的影响。我们假设更严重的炎症状态会导致更强的胆固醇外排能力受损。使用含脂THP1细胞和成纤维细胞,我们能够证明,无论是使用密度梯度超离心分离还是使用载脂蛋白ob沉淀分离,来自严重脓毒症或克罗恩病(活动性或缓解性)患者的HDL外排能力均未受损。然而,脓毒症患者血浆中高密度脂蛋白胆固醇和apoa - 1水平明显较低。基于目前的观察,我们得出结论,炎症性疾病不会干扰HDL介导胆固醇外排的能力。我们的研究结果不支持体外HDL功能变化的生物学相关性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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In Vivo Inflammation Does Not Impair ABCA1-Mediated Cholesterol Efflux Capacity of HDL.

HDL provides atheroprotection by facilitating cholesterol efflex from lipid-laden macrophages in the vessel wall. In vitro studies have suggested impaired efflux capacity of HDL following inflammatory changes. We assessed the impact of acute severe sepsis and mild chronic inflammatory disease on the efflux capacity of HDL. We hypothesize that a more severe inflammatory state leads to stronger impaired cholesterol efflux capacity. Using lipid-laden THP1 cells and fibroblasts we were able to show that efflux capacity of HDL from both patients with severe sepsis or with Crohn's disease (active or in remission), either isolated using density gradient ultracentrifugation or using apoB precipitation, was not impaired. Yet plasma levels of HDL cholesterol and apoA-I were markedly lower in patients with sepsis. Based on the current observations we conclude that inflammatory disease does not interfere with the capacity of HDL to mediate cholesterol efflux. Our findings do not lend support to the biological relevance of HDL function changes in vitro.

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