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与油酸和棕榈酸相比,肉豆蔻烯酸在人内皮细胞中具有更强的抗炎潜力。

Palmitoleic Acid has Stronger Anti-Inflammatory Potential in Human Endothelial Cells Compared to Oleic and Palmitic Acids.

机构信息

Department of Cell and Developmental Biology, University of São Paulo, 1524, Lineu prestes av, São Paulo, Brazil.

Human Development and Health Academic Unit, Faculty of Medicine, Tremona Rd, S016 6HT, University of Southampton, Southampton, UK.

出版信息

Mol Nutr Food Res. 2018 Oct;62(20):e1800322. doi: 10.1002/mnfr.201800322. Epub 2018 Aug 28.

Abstract

SCOPE

Fatty acids (FAs) may affect endothelial cell (EC) function, influencing atherogenesis and inflammatory processes. Palmitoleic acid (POA) has been described as an anti-inflammatory FA. However, its effects on ECs are underexplored. This study compares the effects of POA with those of palmitic acid (PA) and oleic acid (OA) on EC inflammatory responses.

METHODS AND RESULTS

EAHy926 cells (EC lineage) are exposed to PA, OA, or POA, and stimulated with tumor necrosis factor (TNF)-α. Associated with the FA's own incorporation, PA induces a twofold increase in arachidonic acid, while POA increases the amount of cis-vaccenic acid. PA, but not OA, enhances the production of IL-6 and IL-8 in response to TNF-α. In contrast, POA decreases production of monocyte chemotactic protein (MCP)-1, IL-6, and IL-8 compared to PA. TNF-α increases surface intercellular adhesion molecule-1 expression previously decreased by POA. TNF-α stimulation increases the expression of NFκB, cyclooxygenase (COX)-2, MCP-1, and IL-6 genes and reduces the expression of peroxisome proliferator-activated receptor (PPAR)-α gene. PA enhances the expression of MCP-1, IL-6, and COX-2 genes, while POA downregulates these genes, decreases expression of NFκB, and upregulates PPAR-α gene expression.

CONCLUSION

POA has anti-inflammatory effects on ECs stimulated with TNF-α and may counter endothelial dysfunction.

摘要

范围

脂肪酸(FAs)可能影响内皮细胞(EC)功能,影响动脉粥样硬化和炎症过程。棕榈油酸(POA)已被描述为一种抗炎 FA。然而,其对 EC 的影响尚未得到充分探索。本研究比较了 POA 与棕榈酸(PA)和油酸(OA)对 EC 炎症反应的影响。

方法和结果

EAHy926 细胞(EC 系)暴露于 PA、OA 或 POA 中,并接受肿瘤坏死因子(TNF)-α刺激。与 FA 自身掺入相关,PA 诱导花生四烯酸增加两倍,而 POA 增加顺式vaccenic 酸的量。PA 但不是 OA 增强了对 TNF-α的 IL-6 和 IL-8 的产生。相比之下,与 PA 相比,POA 降低了单核细胞趋化蛋白(MCP)-1、IL-6 和 IL-8 的产生。TNF-α 增加了先前被 POA 降低的表面细胞间黏附分子-1 的表达。TNF-α 刺激增加了 NFκB、环氧化酶(COX)-2、MCP-1 和 IL-6 基因的表达,并降低了过氧化物酶体增殖物激活受体(PPAR)-α基因的表达。PA 增强了 MCP-1、IL-6 和 COX-2 基因的表达,而 POA 下调这些基因,降低 NFκB 的表达,并上调 PPAR-α基因的表达。

结论

POA 对 TNF-α刺激的 EC 具有抗炎作用,可能对抗内皮功能障碍。

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