This study examined the effects of phase II metabolism and efflux transportation on the bioavailability of naringin, hesperidin, and their aglycones (naringenin and hesperetin) in rats. Results indicated naringin and hesperidin have a lower oral bioavailability than their aglycones. Of all the phase II enzymes tested, UDP-glucuronosyltransferase (UGT) 1A1, UGT1A2, UGT1A3, UGT1A7 and SULT sulfotransferase (SULT) 1B1 were of minor importance regarding the phase II metabolism of naringenin and hesperetin in the small intestine. Naringin, hesperidin, and their aglycones were all extensively metabolised in the liver. Naringin and hesperidin were more extensively transported by efflux transporters compared to their aglycones. Significant correlations between phase II enzymes and efflux transporters were detected. In conclusion, more extensive metabolism of naringin and hesperidin than their aglycones in the small intestine, and the interplay of phase II enzymes and efflux transporters in the small intestine explain the lower relative oral bioavailability of naringin and hesperidin than their aglycones.

Postbiotics derived from Bacillus species are recognized as promising natural antimicrobial agents. This study aimed to systematically evaluate the inhibitory activity of postbiotics derived from B. velezensis 906 against L. monocytogenes, elucidate the underlying antibacterial mechanisms using agar diffusion assays, broth microdilution, growth kinetics, flow cytometry, phospholipid competition assays, whole-genome mining, and non-targeted metabolomics, and characterize the bioactive metabolites responsible for their antibacterial effects. The postbiotics exhibited significant antagonistic activity against Gram-positive bacteria, Gram-negative bacteria, and fungi. They also inhibited pathogens such as Salmonella and Enterobacter sakazakii. Against L. monocytogenes, the minimum inhibitory concentration was 0.0083 mg/mL. At 1× MIC, the OD600 after 24 h remained at approximately 0.8, compared with 1.3–1.4 in the untreated control, whereas treatment at 4× MIC almost completely inhibited bacterial growth. Mechanistic analyses suggested that the postbiotics interact with membrane phospholipids, resulting in membrane disruption, increased intracellular reactive oxygen species accumulation, and enhanced membrane permeability. Integrated genome mining and non-targeted metabolomics indicated that the antibacterial activity was associated with a coordinated antimicrobial network involving lipopeptides, polyketides, bacteriocin-related compounds, and siderophore-associated metabolites. These findings provide insight into the antibacterial basis of B. velezensis 906 postbiotics and support their potential application in food safety control.