高血糖和高脂血症诱导的T淋巴细胞炎症和氧化应激及ω- 3脂肪酸的有益作用。

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引用次数: 2

摘要

2型糖尿病与高血糖和高脂血症相关;然而,饱和脂肪酸(SFA)与不饱和脂肪酸(UFA)和高糖对人体T淋巴细胞(T细胞)的作用尚不清楚。我们研究了UFA ω-3脂肪酸,α-亚麻酸,对葡萄糖和SFA,棕榈酸,诱导T细胞活化作为高糖和SFA食物炎症过程的有益作用。这些细胞在棕榈酸和/或高糖而不是亚麻酸存在下表现出胰岛素受体(INSR)的浓度和时间依赖性,表达,ROS的产生,脂质过氧化,细胞因子和NF-kB p65易位到细胞核。然而,增加葡萄糖和棕榈酸水平对细胞的激活是附加的,添加亚麻酸以剂量相关的方式抑制葡萄糖和棕榈酸对细胞的激活,并降低氧化应激、脂质过氧化和细胞因子的标记物。我们认为,α-亚麻酸等UFAs可能是一种保护机制,可以防止高糖和SFA食物对糖尿病的高血糖和高脂血症的有害影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hyperglycemia and Hyperlipidemia Induced Inflammation and Oxidative Stress in Human T Lymphocytes and Salutary Effects of ω- 3 Fatty Acid.
Abstract Type 2 Diabetes conditions are associated with hyperglycemia and hyperlipidemia; however, the role of Saturated Fatty Acids (SFA) vs. Unsaturated Fatty Acids (UFA) and high glucose on human T lymphocytes (T cells) is not known. We investigated the salutary effect of the UFA ω-3 fatty acid, α- linolenic acid, on glucose and SFA, palmitic acid, induced activation on T cells as a cause of the inflammatory process with high glucose and SFA foods. These cells in the presence of palmitic acid and/or high glucose but not linolenic acid exhibited a concentration and time-dependent emergence of insulin receptors (INSR), expression, generation of ROS, lipid peroxidation, cytokines and NF-kB p65 translocation to the nucleus. Whereas, activation of the cells by elevated levels of glucose and palmitic acid were additive, addition of linolenic acid in a dose-related manner inhibited activation of cells by glucose and palmitic acid and reduced markers of oxidative stress, lipid peroxidation and cytokines. We propose that UFAs such as α-linolenic acid may serve as a protective mechanism against the deleterious effects of hyperglycemia and hyperlipidemia of high sugar and SFA foods as in diabetes.
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