Huo Jiaying, Pei Wenhao, Liu Guoying, Sun Weizheng, Wu Jihong, Huang Mingquan, Lu Wei, Sun Jinyuan, Sun Baoguo
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.
Foods. 2023 Jan 18;12(3):450. doi: 10.3390/foods12030450.
Several reports have demonstrated that natural polysaccharides exert protective effects on intestinal barrier function. In our previous study, we isolated a polysaccharide named HSP-W from Huangshui (HS). In the present study, the protective role of HSP-W in LPS-induced intestinal barrier dysfunction was determined by several molecular biological techniques. The results showed that HSP-W treatment alleviated the deduced TEER and increased the permeability of intestinal epithelial cells induced by LPS through inhibiting the release of inflammatory cytokines and enhancing the expression of tight junction (TJ) proteins. The underlying molecular mechanisms were elucidated by RNA-seq technique, which indicated that the differentially expressed genes (DEGs) between the LPS-treated and LPS+HSP-W-treated groups were enriched in the "MAPK" signaling pathway. Notably, the overlapping DEGs reversed by HSP-W intervention highlighted the pathways of the "Toll-like receptor" and "NF-B" signaling pathways. The suppression of p38 and NF-B were mediated by the inhibition of MyD88. Furthermore, HSP-W treatment prevented the translocation of NF-B to nucleus, thus inhibiting the release of TNF-, IL-6, and IL-1. Overall, HSP-W has beneficial effects on LPS-induced inflammation; it protects the intestinal barrier from injury in Caco-2 cells through inhibiting the TLR4/MyD88/NF-B and p38 MAPK signaling pathways.
多项报告表明，天然多糖对肠道屏障功能具有保护作用。在我们之前的研究中，我们从黄水（HS）中分离出一种名为HSP-W的多糖。在本研究中，通过多种分子生物学技术确定了HSP-W在脂多糖（LPS）诱导的肠道屏障功能障碍中的保护作用。结果表明，HSP-W处理通过抑制炎性细胞因子的释放和增强紧密连接（TJ）蛋白的表达，减轻了LPS诱导的跨上皮电阻（TEER）降低，并增加了肠道上皮细胞的通透性。通过RNA测序技术阐明了潜在的分子机制，结果表明，LPS处理组和LPS + HSP-W处理组之间的差异表达基因（DEG）在“丝裂原活化蛋白激酶（MAPK）”信号通路中富集。值得注意的是，HSP-W干预逆转的重叠DEG突出了“Toll样受体”和“核因子-κB（NF-κB）”信号通路。p38和NF-κB的抑制是由髓样分化因子88（MyD88）的抑制介导的。此外，HSP-W处理可防止NF-κB易位至细胞核，从而抑制肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和白细胞介素-1（IL-1）的释放。总体而言，HSP-W对LPS诱导的炎症具有有益作用；它通过抑制Toll样受体4（TLR4）/MyD88/NF-κB和p38丝裂原活化蛋白激酶（MAPK）信号通路，保护Caco-2细胞中的肠道屏障免受损伤。
