Mechanistic insights into <i>N</i> -nitrosamine compounds and food-based interventions: a network toxicology and molecular docking study

<i>N</i>-Nitroso compounds (NOCs) are ubiquitous environmental toxicants, yet the molecular pathways through which they initiate gastric cancer (GC), sleep disorders (SD), dysphagia and atherosclerosis (AS) remain poorly defined. This work first sought to delineate the common molecular axis through which NOCs drive GC, SD, dysphagia and AS, and subsequently to leverage that axis for rational prediction and validation of dietary bioactives for translational prevention. Putative NOC-disease interactomes were first reconstructed by network analysis; bioactive food compounds were then retrieved from DSigDB (enrichment <i>p</i> < 0.01) and their binding affinities toward the top-ranked hub were evaluated by molecular docking. NFKB1 emerged as the common central node across all four disease networks, with NOCs predicted to exert toxicity via NF-κB-driven inflammation and impairment of the ubiquitin-proteasome system. Nine model NOCs and eight dietary compounds displayed favorable binding energies (<0 kcal mol^-1) to NFKB1, indicating high target affinity. Collectively, our findings reveal a shared NF-κB-centered pathway underpinning NOC-induced GC, SD, dysphagia and AS, and provide an experimentally tractable panel of dietary bioactives for future preventive intervention.