Sodium humate alleviates LPS-induced intestinal barrier injury by improving intestinal immune function and regulating gut microbiota.

Sodium humate (HNa), known for its abundant functional active groups, is extensively utilized in food dietary supplements due to its versatile properties. Furthermore, HNa possesses notable anti-inflammatory, antioxidant, and anti-diarrheal properties. This research endeavor aimed to elucidate the protective effects of HNa against intestinal barrier injury induced by lipopolysaccharide (LPS). The findings of this study demonstrated that pretreatment with HNa effectively mitigated intestinal barrier injury in the jejunum. HNa exhibited inhibitory effects on the activation of the NLRP3 inflammasome and the production of inflammatory factors within the intestine. HNa supplementation also contributed to the upregulation of mucin and tight junctions (TJs) expression, consequently enhancing the integrity of the intestinal barrier. Notably, our investigation revealed that HNa shared comparable efficacy with the TLR4 inhibitor TAK-242 in inhibiting the TLR4/NFκB signaling pathway. Furthermore, an in-depth analysis of the gut microbiota demonstrated that HNa exerted a regulatory influence on LPS-induced microflora disturbance. In conclusion, these findings collectively indicate that HNa mitigates LPS-induced mucosal damage in the jejunum and preserves the integrity of the intestinal barrier by modulating intestinal immune function and regulating gut microbiota. • HNa increases mucin and tight junctions (TJs) expression and maintains the integrity of the intestinal barrier. • HNa inhibited the NLRP3 inflammasome activation and inflammatory factor expression. • HNa shares the same efficacy with the TLR4 inhibitor TAK-242 in inhibiting the TLR4/NFκB signaling pathway. • HNa regulated gut microbiota and increased the abundance of beneficial bacteria Lactobacillus. [ABSTRACT FROM AUTHOR]