Protective Effects of Fructus Mume Extract Against Deoxynivalenol-Induced Intestinal and Liver Injury in Mice

Deoxynivalenol (DON), a prevalent mycotoxin, induces intestinal and hepatic injury. Fructus mume extract (FME) possesses bioactive properties, yet its protective role against DON remains unclear. This study aimed to investigate the protective mechanisms of FME in DON-challenged mice. Male C57BL/6 mice were divided into control, DON (3 mg/kg), and DON with low-, medium-, or high-dose FME groups for 4 weeks. Analyses included histopathology, UPLC-Q-TOF-MS, network pharmacology, biochemistry, qRT-PCR, immunohistochemistry, a TUNEL assay, metagenomics, and metabolomics. FME significantly alleviated growth inhibition and tissue damage. Among the 38 components identified by UPLC-Q-TOF-MS, all 38 acted on 156 genes, including IL-1β, caspase3, and BAX, to alleviate DON-induced intestinal and hepatic injury. FME enhanced hepatic antioxidant capacity and reduced inflammation by suppressing NF-κB signaling. FME upregulated tight junction proteins, inhibited apoptosis, and restored microbial diversity by enriching beneficial bacteria. Metabolomics revealed FME reversed DON-induced metabolic disruptions in the liver. Correlation analysis indicated FME remodeled the microbiota–liver metabolite network. In conclusion, FME attenuates DON-induced intestinal injury by modulating the gut–liver axis through antioxidant, anti-inflammatory, and anti-apoptotic activities.