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中国精品科技期刊2020
蔡瑞鑫,陈小蝶,朱海彬,等. 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[J]. 华体会体育,2025,46(1):1−7. doi: 10.13386/j.issn1002-0306.2024010151.
引用本文: 蔡瑞鑫,陈小蝶,朱海彬,等. 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[J]. 华体会体育,2025,46(1):1−7. doi: 10.13386/j.issn1002-0306.2024010151.
CAI Ruixin, CHEN Xiaodie, ZHU Haibin, et al. Alpha-Linolenic Acid Attenuates Inflammatory Response in LPS-stimulated Macrophages by Regulating TLR4/MyD88/NF-κB Signaling Pathway[J]. Science and Technology of Food Industry, 2025, 46(1): 1−7. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2024010151.
Citation: CAI Ruixin, CHEN Xiaodie, ZHU Haibin, et al. Alpha-Linolenic Acid Attenuates Inflammatory Response in LPS-stimulated Macrophages by Regulating TLR4/MyD88/NF-κB Signaling Pathway[J]. Science and Technology of Food Industry, 2025, 46(1): 1−7. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2024010151.

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

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

  • 摘要: ω-3脂肪酸具有自然的抗炎属性,而α-亚麻酸(ALA)是一种人体必需的ω-3脂肪酸,为了阐明其体外抗炎机制,本实验采用脂多糖(LPS)刺激巨噬细胞构建炎症模型,通过测定单核细胞趋化蛋白(MCP-1)、白细胞介素4(IL-4)、白细胞介素13(IL-13)等炎症因子的水平、活性氧(ROS)生成量和炎症信号通路相关蛋白表达情况探讨α-亚麻酸减轻脂多糖诱导的炎症反应的机制。结果表明,α-亚麻酸能显著抑制MCP-1的释放,提高抗炎细胞因子IL-13的分泌水平;同时,α-亚麻酸还可以降低ROS生成量,缓解ROS介导的炎性损伤。此外,α-亚麻酸可以通过增加抗氧化酶SOD的表达,减少MDA的堆积,从而减轻炎症反应中氧化应激的伴随性危害。蛋白印迹分析进一步证实,α-亚麻酸可抑制TLR4、MyD88的表达以及下游p65和IκBα的磷酸化水平。以上结果表明,α-亚麻酸可明显抑制LPS诱导的RAW264.7细胞炎症反应,其机制可能与抑制TLR4/MyD88/NF-κB信号通路激活有关。

     

    Abstract: 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.

     

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