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n-3 PUFA 可改善脂肪酸组成,预防软脂酸诱导的细胞凋亡,并在体外和体内差异调节 B 细胞细胞因子的分泌。

n-3 PUFA improves fatty acid composition, prevents palmitate-induced apoptosis, and differentially modifies B cell cytokine secretion in vitro and ex vivo.

机构信息

Department of Biochemistry and Molecular Biology, East Carolina Diabetes and Obesity Institute, Brody School of Medicine, East Carolina University, 600 Moye Blvd, Brody 5S-18, Greenville, NC 27834, USA.

出版信息

J Lipid Res. 2010 Jun;51(6):1284-97. doi: 10.1194/jlr.M000851. Epub 2010 Jan 13.

Abstract

n-3 polyunsaturated fatty acids (PUFAs) modify T-cell activation, in part by remodeling lipid composition; however, the relationship between n-3 PUFA and B-cell activation is unknown. Here we tested this relationship in vitro and ex vivo by measuring upregulation of B-cell surface molecules, the percentage of cells activated, and cytokine secreted in response to lipopolysaccharide (LPS) activation. In vitro, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) improved the membrane n-6/n-3 PUFA ratio, and DHA lowered interleukin (IL)-6 secretion; overall, n-3 PUFAs did not suppress B-cell activation compared with BSA, oleate, or elaidate treatment. Palmitate treatment suppressed the percentage of B cells activated through lipoapoptosis, which was differentially prevented by cosupplementing cells with MUFAs and PUFAs. Ex vivo, we tested the hypothesis with mice fed a control or high-fat saturated, hydrogenated, MUFA or n-3 PUFA diets. n-3 PUFAs had no effect on the percentage of B cells activated. Unexpectedly, the n-3 PUFA diet increased B-cell CD69 surface expression, IL-6 and IFNgamma secretion, and it significantly increased body weight gain. Overall, we propose that changes in lipid composition with n-3 PUFA and suppression of lymphocyte activation is not universal. The study highlights that high-fat n-3 PUFA diets can promote pro-inflammatory responses, at least from one cell type.

摘要

n-3 多不饱和脂肪酸 (PUFA) 通过重塑脂质组成来调节 T 细胞的激活,但 n-3 PUFA 与 B 细胞激活的关系尚不清楚。在此,我们通过测量 B 细胞表面分子的上调、激活细胞的百分比以及对脂多糖 (LPS) 激活的细胞因子分泌,在体外和体内检测了这种关系。在体外,二十碳五烯酸 (EPA) 和二十二碳六烯酸 (DHA) 改善了细胞膜 n-6/n-3 PUFA 比值,并且 DHA 降低了白细胞介素 (IL)-6 的分泌;总体而言,与 BSA、油酸盐或反油酸处理相比,n-3 PUFA 并没有抑制 B 细胞的激活。棕榈酸处理通过脂凋亡抑制 B 细胞的激活百分比,这可以通过细胞共补充 MUFA 和 PUFA 来有差异地预防。在体内,我们用喂食对照或高脂肪饱和、氢化、MUFA 或 n-3 PUFA 饮食的小鼠来测试这一假说。n-3 PUFA 对激活的 B 细胞百分比没有影响。出乎意料的是,n-3 PUFA 饮食增加了 B 细胞 CD69 表面表达、IL-6 和 IFNγ 的分泌,并且显著增加了体重增加。总的来说,我们提出 n-3 PUFA 改变脂质组成和抑制淋巴细胞激活并不是普遍的。该研究表明,高脂肪 n-3 PUFA 饮食至少可以促进一种细胞类型的促炎反应。

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