Dihydromyricetin alleviates intestinal inflammation by changing intestinal microbial metabolites and inhibiting the expression of the MyD88/NF‐κB signaling pathway

Abstract

Inflammatory bowel disease (IBD), a common chronic gastrointestinal disease in humans, has emerged as a global public health challenge. Dihydromyricetin (DHM) has anti‐inflammatory and antioxidant activities, which can alleviate inflammation. In this study, we explored the effect and underlying mechanism of DHM on dextran sulfate sodium (DSS)‐induced colitis in mice and porcine jejunum epithelial cells (IPEC‐J2) exposed to lipopolysaccharide (LPS). We found that DHM alleviated loss of weight, diarrhea, and damage of colon structure in colitis mice. For the intestinal microbial, a significant rise in the amount of the potentially beneficial genera and a decline in the amount of harmful genera were observed in DHM‐treated colitis mice. Metabolomic analysis of cecal content revealed that DHM restored phenylalanine metabolism, arginine biosynthesis, and arachidonic acid metabolism disorders caused by intestinal inflammation. Moreover, DHM decreased the level of pro‐inflammatory cytokines and reactive oxygen species in LPS‐treated IPEC‐J2 cells. DHM also reduced the expression of MyD88 and nuclear factor‐κB (NF‐κB). In summary, we found that 125 mg/kg DHM administration alleviated diarrhea, reinstated intestinal barrier function, modulated intestinal dysbiosis, and suppressed the expression of myeloid differentiation factor 88 (MyD88) and NF‐κB. Therefore, DHM may be a potentially therapeutic agent for IBD.

Oleanolic acid alleviate intestinal inflammation by inhibiting Takeda G-coupled protein receptor (TGR) 5 mediated cell apoptosis

“…18 Extracts from apple peel and tea have also been found to have the ability to alleviate IBD. 29,30 In recent years, triterpenoids such as maslinic acid in food have the potential to inhibit colorectal cancer. 31 Accumulating evidence implicates bile acid receptors as pivotal factors in intestinal epithelial repair.…”

Anti-Proteolytic Peptide R7I Protects the Intestinal Barrier and Alleviates Fatty Acid Malabsorption in Salmonella typhimurium-Infected Mice

“…LPS can interact with TLR4/MD2 to create a complex that specifically activates the MyD88-dependent pathway, which in turn activates the transcription factor NF-κB [33]. NF-κB, as a key signaling molecule, regulates numerous genes for different processes of the immune and inflammatory responses [34]. Inflammatory substances like IL-1β, IL-6, and TNF-α are released in huge quantities as a result of NF-κB activation, harming the animal's body [35].…”