TLR4型
MAPK/ERK通路
信号转导
p38丝裂原活化蛋白激酶
NF-κB
细胞生物学
碳酸钙-2
脂多糖
肿瘤坏死因子α
炎症
Toll样受体
肠上皮
化学
势垒函数
生物
受体
生物化学
免疫学
先天免疫系统
细胞
上皮
遗传学
作者
Jiaying Huo,Wenhao Pei,Guoying Li,Weizheng Sun,Jihong Wu,Mingquan Huang,Wei Lü,Jinyuan Sun,Baoguo Sun
出处
期刊:Foods
[Multidisciplinary Digital Publishing Institute]
日期:2023-01-18
卷期号:12 (3): 450-450
被引量:1
标识
DOI:10.3390/foods12030450
摘要
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-κB” signaling pathways. The suppression of p38 and NF-κB were mediated by the inhibition of MyD88. Furthermore, HSP-W treatment prevented the translocation of NF-κB to nucleus, thus inhibiting the release of TNF-α, IL-6, and IL-1β. 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-κB and p38 MAPK signaling pathways.
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