Mechanism of Polygonati Rhizoma in Treatment of Gout Based on Network Pharmacology

OBJECTIVE To predict the targets and pathways for the main active components of Polygonati Rhizoma in the treatment of gout based on network pharmacology and molecular docking. METHODS The active components and targets of Polygonati Rhizoma were obtained by TCMSP database and Drugbank database. Gout-related target genes were obtained using the TTD database, OMIM database and GeneCards database. Gout-related disease genes and targets of Polygonati Rhizoma were imported into Venny 2.1 to select the targets of Polygonati Rhizoma for gouty treatment. The network map of “TCM-component-target-disease” was constructed using Cytoscape 3.8.0 software. Polygonati Rhizoma-gout common targets were input into the STRING database to build the PPI network. GO and KEGG pathway enrichment analysis was performed using Metascape database, and molecular docking was performed with Autodock_vina software. Finally, The prediction results were verified by preparing an in vitro gout model of RAW264.7 cells induced by LPS combined with MSU. RESULTS Thirteen active components, 90 potential targets, 1 139 gout-related disease targets and 19 effective targets(including MAPK14, CAT, PPARG, NOS2, VEGFA, etc.) for gout control of Polygonati Rhizoma were predicted. The mechanism might be related to PI3K-Akt signaling pathway, platelet activation, calcium signaling pathway and estrogen signaling pathway. Molecular docking results showed that the binding energy of the active component to the core target was -10.4 ~ -4.6 kcal·mol^-1, which had a good binding ability. Cell experiments further showed that diosgenin was able to reduce the expressions of p38 MAPK and its upstream ERK1/2 phosphorylated protein. CONCLUSION The prevention and treatment mechanism of Polygonati Rhizoma against gout might be related to the core target MAPK14.