Research on the mechanism of action of the Li Qi Dao Tan Decoction in the treatment of schizophrenia based on network pharmacology and molecular docking.

This study explores the potential targets and signaling pathways of the Li Qi Dao Tan Decoction (LQDTD) in the treatment of schizophrenia using network pharmacology and molecular docking technology. The traditional Chinese medicine systems pharmacology database and analysis platform database was searched to obtain the active ingredients and targets of the LQDTD. Databases such as GeneCards, DrugBank, and OMIM were searched for schizophrenia-related disease targets. By drawing a Venn diagram, the intersection targets of LQDTD and schizophrenia were obtained. The STRING database was used to construct the protein-protein interaction. The online tool of the DAVID database was used to analyze the gene ontology and Kyoto Encyclopedia of Genes and Genomes pathways of the intersection targets of LQDTD and schizophrenia. The Cytoscape software was employed to construct the network of traditional Chinese medicine ingredients, targets, and pathways. AutoDock, Chem3D, and PyMOL software facilitated molecular docking and the calculation of binding energy for the identified key active ingredients and targets, from which the 7 pairs with the lowest binding energy were selected. PyMOL was utilized for analysis and visualization. We identified 5 active ingredients of LQDTD: luteolin, nobiletin, baicalin, quercetin and licochalcone A. Key proteins, including signal transducer and activator of transcription 3, TP53, and EGFR, were identified through the protein-protein interaction map. Kyoto Encyclopedia of Genes and Genomes analysis indicated that the pathways involved primarily included lipid and atherosclerosis pathways, hepatitis B virus-related pathways, AGE-RAGE signaling pathways, Chemical carcinogenesis receptor activation, and prostate cancer signaling pathways. The treatment of schizophrenia may influence key proteins such as signal transducer and activator of transcription 3, TP53, and EGFR, intervening in lipid and atherosclerotic pathways, hepatitis B virus-related pathways, AGE-RAGE signaling pathways, chemical carcinogenesis receptor activation, and prostate cancer signaling pathways. However, the exact mechanisms of action require further experimental verification.