The oral bioavailability of curcumin is inherently low, which significantly limits its application in food systems. The objective of this study was to evaluate the impact of high-pressure processing on the stability and bioaccessibility of curcumin within an emulsion gel during simulated gastrointestinal transit and to assess its cellular uptake. Our findings suggest that increasing pressure levels and high κ-carrageenan concentrations can enhance the stability of the curcumin delivery system. Elevated κ-CG concentrations were found to retard the action of proteases on dissociating protein molecules from the gel network. The emulsion gel effectively slowed the release of free fatty acids and reduced the curcumin release rate during the gastric phase. Scanning electron microscopy images revealed that higher pressures induced the formation of a more uniform and dense network structure in the gel. While the gel network structures were well-preserved after gastric digestion, they were disrupted into smaller particles following intestinal digestion, with particle size increasing with higher applied pressures. Cytotoxicity assays indicated that the digesta from the intestinal phase was highly toxic to Caco-2 cells. Among the tested samples, the emulsion gel prepared with 1.0% κ-CG at 600 MPa demonstrated the highest curcumin bioavailability, reaching 63.82 ± 7.10%. These findings underscore the potential of HPP-induced emulsion gels as a viable delivery system for enhancing curcumin bioaccessibility and cellular uptake.

Almond-derived peptide fractions (APs) represent a promising yet underexplored class of plant-based bioactive compounds for ulcerative colitis (UC) management. This study investigated the protective effects of APs against dextran sulfate sodium (DSS)-induced colitis in male BALB/c mice using integrated 16S rRNA sequencing and transcriptomic analysis. Mice received low-dose (200 mg/kg) or high-dose (400 mg/kg) APs during 7-day DSS administration. Both doses significantly attenuated body weight loss, disease activity index, colon shortening, and histopathological damage. Compared with the DSS group, low-dose and high-dose APs reduced disease activity index by 65.9% and 52.4%, increased colon length by 30.0% and 26.5%, decreased histopathological scores by 39.6% and 55.1%, and lowered colonic myeloperoxidase activity by 13.9% and 34.1%, respectively. APs also modulated inflammatory cytokines, improved mucus-barrier-related indices, and enhanced continuous ZO-1 localization at epithelial junctions. Additionally, 16S rRNA sequencing indicated that AP treatment was associated with altered genus-level microbiota profiles after DSS exposure, including changes in Ligilactobacillus, Escherichia-Shigella, and Parabacteroides-related taxa. Transcriptomic analysis suggested dose-associated response patterns: low-dose APs were associated with broader immune-related transcriptional changes, whereas high-dose APs were more closely associated with extracellular matrix organization, focal adhesion, and genes enriched in the PI3K-Akt signaling pathway. These findings support the protective effects of APs in DSS-induced acute colitis and suggest potential associations among microbiota alterations, host transcriptional responses, and mucosal repair.