Alpha-Linolenic Acid Attenuates Inflammatory Response in LPS-stimulated Macrophages by Regulating TLR4/MyD88/NF-κB Signaling Pathway

被引：0

作者：

α-亚麻酸通过TLR4/MyD88/NF-κB信号通路抑制脂多糖诱导的巨噬细胞炎症

机构：

[1] State Key Laboratory of Food Science and Resources, Nanchang University, Nanchang

来源：

Shen, Mingyue (shenmingyue1107@163.com) | 2025年 / 46卷 / 01期

关键词：

inflammation; macrophage; signaling pathways; α-linolenic acid;

D O I：

10.13386/j.issn1002-0306.2024010151

中图分类号：

学科分类号：

摘要：

Omega-3 fatty acids have natural anti-inflammatory properties, and α-linolenic acid (ALA) is an essential ω-3 fatty acid. In order to elucidate its anti-inflammatory mechanism in vitro, lipopolysaccharide (LPS) was used to stimulate macrophages to construct an inflammatory model. The levels of monocyte chemotactic protein (MCP-1), interleukin4 (IL-4), interleukin13 (IL-13), the production of reactive oxygen species (ROS) and the expression of related proteins in inflammatory signaling pathways were determined to explore the mechanism of α-linolenic acid in alleviating LPS-induced inflammatory response. The results showed that α-linolenic acid significantly inhibited the release of MCP-1 and increased the secretion level of anti-inflammatory cytokine IL-13. At the same time, α-linolenic acid also reduced ROS production and alleviated ROS-mediated inflammatory damage. In addition, α-linolenic acid could reduce the accumulation of MDA by increasing the expression of antioxidant enzymes SOD, thereby reducing the concomitant harm of oxidative stress in inflammatory responses. Western blot analysis further confirmed that α-linolenic acid inhibited the expression of TLR4, MyD88, and phosphorylation levels of downstream p65 and IκBα. These results indicate that α-linolenic acid can significantly inhibit the LPS-induced inflammatory response of RAW264.7 cells, and the mechanism may be related to inhibiting the activation of TLR4/MyD88/NF-κB signaling pathway. © The Author(s) 2025.

引用

页码：377 / 383

页数：6

共 29 条

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