Huangshui Polysaccharide Exerts Intestinal Barrier Protective Effects through the TLR4/MyD88/NF-κB and MAPK Signaling Pathways in Caco-2 Cells

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-kappa B signaling pathways. The suppression of p38 and NF-kappa B were mediated by the inhibition of MyD88. Furthermore, HSP-W treatment prevented the translocation of NF-kappa B to nucleus, thus inhibiting the release of TNF-alpha, IL-6, and IL-1 beta. 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-kappa B and p38 MAPK signaling pathways.

Automated summary

Natural polysaccharide HSP-W from Huangshui was found to protect intestinal barrier function by inhibiting the release of inflammatory cytokines and enhancing tight junction protein expression. Furthermore, HSP-W exerted its effects through the inhibition of the TLR4/MyD88/NF-kappa B and p38 MAPK signaling pathways.