Key Laboratory of Brewing Molecular Engineering of China Light Industry, Beijing Technology and Business University, Beijing 100048, China; School of Food Science and Engineering, South China University of Technology, Guangzhou 510640, China; Beijing Laboratory of Food Quality and Safety, Beijing Technology and Business University, Beijing 100048, China.
Key Laboratory of Brewing Molecular Engineering of China Light Industry, Beijing Technology and Business University, Beijing 100048, China; Beijing Laboratory of Food Quality and Safety, Beijing Technology and Business University, Beijing 100048, China.
Food Res Int. 2022 Dec;162(Pt B):112175. doi: 10.1016/j.foodres.2022.112175. Epub 2022 Nov 19.
Polysaccharides from Huangshui (HS) have the function of antioxidant and immunoregulation, but its intestinal barrier protection activity and the underlying mechanism remains unclear. The present work mainly studied the intestinal barrier protection function and its potential molecular mechanism of a heteropolysaccharide named NLS-2 with a molecular weight of 51.9 kDa. NLS-2 reduced intestinal permeability by decreasing the content of inflammatory cytokines and increasing the expression of tight junction (TJ) protein in LPS-damaged Caco-2 cells, thus protecting the intestinal barrier function. RNA-seq results showed that the differentially expressed genes (DEGs) were mainly enriched in the signaling pathways of MAPK, Toll-like receptor, and NF-κB. Subsequent western blot validation experiments proved that NLS-2 could indeed inhibit the two pathways of MAPK and NF-κB by reducing the expression of TRL4, thereby down-regulating the release of downstream pro-inflammatory cytokines and playing the role of intestinal barrier protection. Collectively, NLS-2 has beneficial effects on LPS-damaged intestinal barrier by inhibiting the TRL4/MyD88/NF-κB and MAPK signaling pathways.
黄水（HS）多糖具有抗氧化和免疫调节功能，但它的肠道屏障保护活性及其潜在的机制尚不清楚。本工作主要研究了一种相对分子质量为 51.9 kDa 的杂多糖 NLS-2 的肠道屏障保护功能及其潜在的分子机制。NLS-2 通过降低 LPS 损伤的 Caco-2 细胞中炎症细胞因子的含量和增加紧密连接（TJ）蛋白的表达来降低肠道通透性，从而保护肠道屏障功能。RNA-seq 结果表明，差异表达基因（DEGs）主要富集在 MAPK、Toll 样受体和 NF-κB 的信号通路中。随后的 Western blot 验证实验证明，NLS-2 可以通过降低 TLR4 的表达来抑制 MAPK 和 NF-κB 这两条通路，从而下调下游促炎细胞因子的释放，发挥肠道屏障保护作用。综上所述，NLS-2 通过抑制 TLR4/MyD88/NF-κB 和 MAPK 信号通路对 LPS 损伤的肠道屏障具有有益作用。
