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首页> 外文期刊>The Journal of Nutritional Biochemistry >Excessive dietary linoleic acid induces proinflammatory markers in rats
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Excessive dietary linoleic acid induces proinflammatory markers in rats

机译：饮食中过量的亚油酸会诱发大鼠促炎性标志物

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摘要

Following the historical dietary recommendations, the substitution of polyunsaturated fatty acids (PUFAs) for saturated fatty acids (SFAs) resulted in a dramatic increase of linoleic acid (LA) in the Western diet. While proatherogenic properties of SFAs have been described, the involvement of LA on the inflammatory process remains controversial. Herein, we evaluated the effects of an excessive LA intake on the cytokine-induced expression of endothelial adhesion molecules vascular cell adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1), through the nuclear factor (NF)-kappa B pathway, in comparison with a control diet and regarding a "positive" SFA diet. Wistar rats were fed experimental diets a control diet or diets enriched with LA or SFA for 11 weeks. Plasma lipid parameters and proinflammatory cytokine production such as interleukin-1 beta and tumor necrosis factor (TNF)-alpha were analyzed. Expression of endothelial adhesion molecules and NF-kappa B was determined by immunohistochemical analysis. No difference was observed in body weight. The enriched diets did not affect triglyceride and total cholesterol levels in plasma. Our results demonstrated that excessive dietary LA intake increased TNF-alpha levels (P.05) in plasma. Rats fed the IA-enriched diet showed a significantly higher expression of VCAM-1, ICAM-1 and NF-kappa B in aortas. In addition, our results demonstrated that an excess of LA is more efficient to activate endothelial molecular process than an excess of SFA. The present study provides further support for the proinflammatory properties of LA and suggests an LA-derivatives pathway involved in the inflammatory process. (C) 2015 Elsevier Inc. All rights reserved.
机译：根据历史上的饮食建议，用多不饱和脂肪酸（PUFA）代替饱和脂肪酸（SFA）导致西方饮食中亚油酸（LA）的急剧增加。尽管已经描述了SFA的促动脉粥样硬化特性，但LA与炎症过程的关系仍然存在争议。在这里，我们通过核因子评估了过量摄入LA对细胞因子诱导的内皮粘附分子血管细胞粘附分子1（VCAM-1）和细胞间细胞粘附分子1（ICAM-1）表达的影响。与对照饮食相比，以及关于“阳性” SFA饮食，NF-κB途径。向Wistar大鼠喂食实验饮食，对照饮食或富含LA或SFA的饮食11周。分析血浆脂质参数和促炎细胞因子的产生，例如白介素-1β和肿瘤坏死因子（TNF）-α。通过免疫组织化学分析确定内皮粘附分子和NF-κB的表达。体重没有差异。丰富的饮食不影响甘油三酸酯和血浆中的总胆固醇水平。我们的结果表明，饮食中过多的LA摄入会增加血浆中的TNF-α水平（P <.05）。饲喂富含IA的饮食的大鼠在主动脉中显示出明显更高的VCAM-1，ICAM-1和NF-κB表达。此外，我们的结果表明，与过量的SFA相比，过量的LA可以更有效地激活内皮分子过程。本研究为LA的促炎特性提供了进一步的支持，并提出了LA衍生物途径参与炎症过程。 （C）2015 Elsevier Inc.保留所有权利。

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