Using network pharmacology and molecular docking to investigate the mechanism of action of the active components of agarwood moxibustion therapy for the treatment of chronic atrophic gastritis.

Chronic atrophic gastritis (CAG) is a long-term inflammatory condition of the gastric mucosa characterized by glandular atrophy, intestinal metaplasia and reduced acid secretion, often considered a precancerous lesion of the stomach. This study utilized a combined network pharmacology and molecular docking approach to elucidate the mechanisms of moxibustion therapy against CAG. Disease-related targets were retrieved from GeneCards, OMIM, PharmaGkb, TTD and DrugBank, while moxibustion's active components and their targets were sourced from TCMSP database. Overlapping targets between the drug and disease were identified, representing potential therapeutic targets. Cytoscape was employed to construct component-target networks and R was used for GO and KEGG enrichment analyses. STRING database facilitated protein-protein interaction network construction and identification of key targets. Molecular docking, via AutoDock, validated component-target interactions. Eighteen common targets were identified from 379 drug targets and 361 disease targets, linked to 18 active components. Topological analysis pinpointed TP53, IL-1β, PTGS2, CXCL8, CASP8 and STAT1 as crucial targets. KEGG enrichment revealed involvement of TNF-κB, p53, IL-17 and Toll-like receptor signaling pathways. Molecular docking confirmed stable binding between key components and targets. These findings suggest that moxibustion's therapeutic effects on CAG are mediated through modulation of immune, inflammatory and tumor-related pathways.