Unveiling sialylation-related hub genes mediating protective effects of curcumin against intestinal inflammation.

This study employed an integrated bioinformatics approach to characterize sialylation-associated hub genes underlying curcumin's (CUR) therapeutic efficacy in intestinal inflammation. Transcriptomic analysis of GSE180491 datasets revealed 449 differentially expressed genes (DEGs; 275 downregulated and 174 upregulated) in CUR-treated murine colitis, including 58 sialylation-related DEGs (53 downregulated and 5 upregulated) curated from GeneCards. Through synergistic application of functional enrichment (DAVID/PANTHER), protein interactome mapping (STRING/Cytoscape), and topological analysis (CytoHubba), we identified six central regulators (VCAM1, ICAM1, TLR2, CXCL1, IL33, and FCGR2B) orchestrating CUR-mediated anti-inflammatory responses. Mechanistic profiling demonstrated these targets modulate three critical axes: 1) innate immunity through TLR/IL-17/chemokine signaling, 2) epithelial barrier integrity via focal adhesion/PI3K-Akt pathways, and 3) immunometabolic reprogramming involving TNF-α/cytokine regulation. The sialylation network showed significant enrichment in IBD-associated pathways (necroptosis, leukocyte transendothelial migration) and proteolytic modulation mechanisms. Our findings not only establish sialylation modification as a novel pharmacological target for CUR but also provide a computational framework bridging phytochemical intervention with precision mucosal immunology, offering translational potential for dietary prevention and targeted therapy of gut inflammation.