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首页> 外文期刊>Molecular Nutrition and Food Research >Metabolism and actions of conjugated linoleic acids on atherosclerosis-related events in vascular endothelial cells and smooth muscle cells.
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Metabolism and actions of conjugated linoleic acids on atherosclerosis-related events in vascular endothelial cells and smooth muscle cells.

机译:共轭亚油酸的代谢及其对血管内皮细胞和平滑肌细胞中动脉粥样硬化相关事件的作用。

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摘要

Conjugated linoleic acids (CLAs) are biologically highly active lipid compounds that have attracted great scientific interest due to their ability to cause either inhibition of atherosclerotic plaque development or even regression of pre-established atherosclerotic plaques in mice, hamsters and rabbits. The underlying mechanisms of action, however, are only poorly understood. Since cell culture experiments are appropriate to gain insight into the mechanisms of action of a compound, the present review summarizes data from cell culture studies about the metabolism and the actions of CLAs on atherosclerosis-related events in endothelial cells (ECs) and smooth muscle cells (SMCs), which are important cells contributing to atherosclerotic lesion development. Based on these studies, it can be concluded that CLAs exert several beneficial actions including inhibition of inflammatory and vasoactive mediator release from ECs and SMCs, which may help explain the anti-atherogenic effect of CLAs observed in vivo. The observation that significant levels of CLA metabolites, which have been reported to have significant biological activities, are well detectable in ECs and SMCs indicates that the anti-atherogenic effects observed with CLAs are presumably mediated not only by CLAs themselves but also by their metabolites.
机译:共轭亚油酸(CLA)是具有生物高活性的脂质化合物,由于它们具有抑制小鼠,仓鼠和兔子中动脉粥样硬化斑块发展甚至使预先建立的动脉粥样硬化斑块消退的能力,因此引起了极大的科学兴趣。然而,人们对其作用的基本机制了解甚少。由于细胞培养实验适合深入了解化合物的作用机理,因此本综述总结了细胞培养研究的数据,这些数据涉及代谢和CLA对内皮细胞(ECs)和平滑肌细胞中动脉粥样硬化相关事件的作用(SMC),这是有助于动脉粥样硬化病变发展的重要细胞。基于这些研究,可以得出结论,CLA发挥了几种有益的作用,包括抑制EC和SMC释放的炎症和血管活性介质,这可能有助于解释在体内观察到的CLA的抗动脉粥样硬化作用。在EC和SMC中可以很好地检测到据报道具有重要生物学活性的大量CLA代谢产物的观察结果表明,用CLA观察到的抗动脉粥样硬化作用可能不仅由CLA本身介导,而且还由其代谢产物介导。

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