Mechanism of

Background: Methods: Target genes of RS and influenza A were attained by accessing network databases. We then determined the intersection of both genes through bioinformatics using R and Perl language. The protein-protein interaction (PPI) network was constructed by the STRING website (https://cn.string-db.org). The network analysis was done using Cytoscape software. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were applied for the above genes. Effective components as core targets were screened out based on the condition that the interaction must come first. These core targets were combined with 3D structures of main RNA coding proteins of influenza A virus. Molecular docking was used to visualize drug-target interaction via AutoDock Vina and PyMOL. Results: Twenty-eight active components and 40 target genes were acquired through the regulatory network of active components of RS and the PPI network. Seventy-one bioinformatics expressions were obtained through GO enrichment analysis (P<0.05). A total of 124 signaling pathways were screened by KEGG enrichment analysis (P<0.05). Acacetin, wogonin, baicalein, oroxylin A, and beta-sitosterol, which are rich in RS, are closely related to hemagglutinin (HA), NeurAminidase (NA), nucleoprotein (NP), polymerase basic protein 1 (PB1), polymerase basic protein 2 (PB2), polymerase acidic (PA), matrix protein 1 (M1), matrix protein 2 (M2), and non-structural protein (NS), which are the main RNA coding proteins of influenza A virus. The binding energies of these 8 proteins were less than -5 kJ/mol, indicating that the ligands had strong affinity with receptor proteins. Conclusions: RS is rich in core target compounds, and its mechanism of action is further expressed. It could have a good therapeutic effect for influenza A through multi-compound and multi-target regulation of these specific protein targets, and targets and pathways related to immunity and inflammation.