Phlorizin Alleviates Inflammation Caused by Deoxynivalenol by Regulating the Gut Microbiome and Inhibiting the TLR4/MyD88/NF-κB Signaling Pathway in Mice

Deoxynivalenol (DON) is a commonly seen mycotoxin that can cause various health problems, such as vomiting, growth retardation, and immunosuppression, in both humans and animals due to its ability to affect the gastrointestinal tract and the immune system. Phlorizin (PHZ) is a polyphenolic compound with anti-inflammatory and antioxidant effects that are present in apples. In this study, we explored the alleviating effects of PHZ against DON-induced adverse effects in mice. The results revealed that coexposure to DON and 200 mg/kg b.w. PHZ significantly alleviated DON-induced liver injury. Further results showed that PHZ upregulated the intestinal tight junction proteins (Claudin, Occludin, and ZO-1), improved intestinal permeability, and inhibited the liver TLR4/NF-kappa B signaling pathway. The latter may explain the alleviated liver inflammation. Analysis of 16S rRNA gene sequencing of intestinal microbiota revealed that PHZ coexposure prevented the intestinal microbiota imbalance caused by DON. PHZ coexposure also prevented an increase of the relative abundance of Bacteroides and Clostridia_UCG-014 and prevented the DON-induced decrease of beneficial bacteria (Duchenella and Roseburia). It is concluded that PHZ coexposure may prevent DON-induced gut and liver inflammation through multiple routines, including regulating intestinal microorganisms, restoring intestinal mucosal barrier function, and improving intestinal permeability. In conclusion, PHZ coadministration is promising to alleviate the toxicity of DON.