Exploration of the mechanism of Baitong decoction in the treatment of cold asthma based on network pharmacology and molecular docking

Abstract

ObjectiveTo investigate the mechanism of Baitong decoction in the treatment of cold asthma through network pharmacology. MethodsThe pharmacological database and analysis platform of the traditional Chinese medicine system (TCMSP) was used to search and screen for active components and potential targets of the three herbs in Baitong decoction (Fuzi, Ganjiang, and Congbai). The asthma disease targets were searched and screened using the GeneCards database and the parts intersecting with the action targets of the Baitong decoction was obtained. The interactions among the various targets were counted on the STRING website. Cytoscape 3.8.2 software was used for network analysis, and R program was used for biological process analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Molecular docking between drug components and targets was performed using the Protein Data Bank (PDB) and PubChem website, and Autodock and PyMOL software. ResultsForty-seven key target genes of Baitong decoction were found to interfere with cold asthma. The final core targets are JUN, PTGS2, and HMOX1. Cell biological processes, including oxidative stress, lipopolysaccharide response, heme binding, oxidoreductase activity, and G-protein-coupled amine receptor activity, were studied using Gene Ontology (GO) enrichment analysis. KEGG enrichment analysis revealed that the signaling pathways found in this study included the tumor necrosis factor (TNF), lipid metabolism, and atherosclerosis signaling pathways. The docking results showed that PTGS2 has a high affinity for kaempferol, catechin (+), and deltoin, and that JUN has a great affinity for kaempferol. ConclusionLipopolysaccharide response and the TNF signaling pathway may play a key role in the therapeutic effect of Baitong decoction on cold asthma. Drug components, including kaempferol, catechin (+), and deltoin, may affect the TNF signaling pathway by targeting PTGS2 and JUN, thereby regulating the immune inflammatory response.