Abstract

We aimed to develop novel methods for treating periodontitis by identifying the main targets and pathways of curcumin in treating periodontitis. Potential targets of curcumin and differential genes were obtained from multiple drug databases and gene expression omnibus database chip data, respectively. Common targets of curcumin and periodontitis were screened, a protein-protein interaction network map of these common targets was constructed, and the critical targets were identified. These targets were subjected to gene ontology and Kyoto encyclopedia of genes and genomes enrichment analysis to construct a "curcumin-target-pathway" network. Finally, molecular docking was performed on curcumin and its key targets. We retrieved 115 curcumin-related targets from multiple drug databases. We further identified 376 differential genes and 413 curcumin targets. Among the 2587 targets for periodontitis diseases, 72 common curcumin-periodontitis targets were identified. Notably, AKT serine/threonine kinase 1, tumor protein P53, signal transducer and activator of transcription 3, matrix metallopeptidase 9, caspase-3, epidermal growth factor receptor, epidermal growth factor, cyclin D1, mitogen-activated protein kinase 14, and peroxisome proliferator activated receptor gamma were the key targets of curcumin in periodontitis treatment. Approximately 805 processes, including cellular response to chemical stress, and 39 signaling pathways, including forkhead box O1 signaling pathway, were enriched. All key targets, except tumor protein P53, had a high affinity for curcumin. Curcumin interacts with forkhead box O1, advanced glycosylation end-product specific receptor, mitogen-activated protein kinase, phosphoinositide 3 kinase-protein kinase B, and tumor necrosis factor signaling pathways in diabetic complications via key targets, including AKT serine/threonine kinase 1, mitogen-activated protein kinase 14, epidermal growth factor and epidermal growth factor receptor. Therefore, curcumin may reduce periodontal tissue inflammation and alveolar bone loss by inhibiting inflammatory cytokine expression and promoting osteoclast apoptosis, thereby facilitating periodontitis treatment.