Immune regulation and inflammation inhibition of Arctium lappa L. polysaccharides by TLR4/NF-κB signaling pathway in cells

文献类型: 外文期刊

第一作者: Zeng, Feng

作者: Zeng, Feng;Li, Ying;Zhang, Xiaoxiao;Zhao, Xingyu;Huang, Wuyang;Zeng, Feng;Shen, Li;Huang, Wuyang;Zhang, Xiaoxiao;Zhao, Xingyu;Huang, Wuyang;Beta, Trust;Li, Bin;Chen, Rui;Huang, Wuyang

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关键词: Arctium lappa L.; Burdock roots; Polysaccharides; Immunoregulation; Inflammation; TLR4/NF-kappa B signaling pathway

期刊名称:INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES ( 影响因子:8.2; 五年影响因子:7.8 )

ISSN: 0141-8130

年卷期: 2024 年 254 卷

页码:

收录情况: SCI

摘要: Arctium lappa L. polysaccharides (ALP) are important active ingredients of burdocks with various bioactivities. In the present study, a crude polysaccharide was extracted from A. lappa L. roots and purified using DEAE-52 and Sephacryl (TM) S-400 columns to reach 99 % purity. This neutral polysaccharide contained fructose, glucose, galactose and arabinose in a ratio of 0.675:0.265:0.023:0.016 and had a Mw of 4256 Da. The immunomodulatory activity and intestinal inflammation inhibitory effects of ALP were investigated in in vitro models, including lipopolysaccharide-induced macrophage RAW264.7 and interleukin (IL)-1 beta-induced colon Caco-2 cells. The results revealed that ALP possessed both antioxidant and anti-inflammatory effects by decreasing nuclear factor-E2-related factor 2 mRNA expression and reactive oxygen species. Furthermore, ALP was found to have inhibitory effects on pro-inflammatory cytokines, including IL-8, IL-6, IL-1 beta, and tumor necrosis factor-alpha, as well as inflammatory cytokines, such as intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemoattractant protein-1 by down-regulating the Toll-like receptor 4 (TLR4)/NF-kappa B (nuclear factor-kappa B signaling) pathway. It indicated that A. lappa L. was an ideal source of bioactive polysaccharides having potential to be developed as functional foods or nutraceuticals to improve immune system and prevent/treat intestinal inflammation.

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