Dendrobium officinale Polysaccharides Inhibit CDCA-Induced Gastric Intestinal Metaplasia through Activating NRF2/HO-1 and Modulating HNF4α/CDX2 Signaling Pathway

Bile reflux (BR) was considered to be an independent risk factor for the development of precancerous gastric lesions and GC. Dendrobium officinale polysaccharides (DOP) show a novel potential in preventing the progress of gastric cancer. However, the specific mechanism of DOP that causes such activities remains a mystery. This study aimed to investigate the effects of DOP on chenodeoxycholic acid (CDCA)-induced gastric intestinal metaplasia and explore the underlying mechanisms. Different concentrations of DOP had no significant damage to normal GSE-1 cells and gastric intestinal metaplasia model cells by CCK-8 assay. After DOP treatment, the mRNA and protein expression of CDX2 (p < 0.01) and HNF4 alpha (p < 0.01) were decreased, and HO-1 (p < 0.05) and TFF2 (p < 0.01) were increased. The NRF2 protein expression was slightly upregulated (p < 0.05), and H-DOP further promoted NRF2 protein expression in the nucleus (p < 0.05). Hence, our findings reveal that DOP could be used as a potential anti-inflammation supplement by activating NRF2/HO-1 and modulating the HNF4 alpha/CDX2 signaling pathway to inhibit the progress of CDCA-induced gastric intestinal metaplasia.

Automated summary

This study found that Dendrobium officinale polysaccharides (DOP) have the potential to inhibit the progression of gastric intestinal metaplasia induced by chenodeoxycholic acid (CDCA). DOP exerts its anti-inflammatory effects by activating the NRF2/HO-1 signaling pathway and modulating the HNF4 alpha/CDX2 signaling pathway.