Exploration of the Mechanism of Fritillaria Taibaiensis in stopping cough, eliminating phlegm and relieving asthma Based on Network Pharmacology,Molecular Simulation and animal experiments

Background Using network pharmacology and molecular docking methods, this study explores the mechanism of action of Fritillaria Taibaiensis (Taibai Beimu, TB) in relieving cough, asthma, and phlegm, and preliminarily verifies the relevant pathways through animal experiments. Methods Using traditional Chinese medicine database to screen the main components and targets, and obtaining disease targets through disease database, and repeated targets were summarized and deleted before being imported into Cytoscape software to construct a network; Using database to analyze protein-protein interactions of intersecting targets and obtain core targets. Perform enrichment analysis on intersecting targets and construct a "drug component target pathway disease" network; Simultaneously, Maestro software was used for molecular docking to verify the binding ability of the active ingredient to the core target. Animal experiments were conducted to analyze and verify the cough stopping, asthma relieving, and expectorant effects of TB; Western blot verification of its effect on the expression level of target proteins. Results 9 active ingredients and 152 targets were screened, and KEGG pathway enrichment predicted that drugs mainly exert their effects through signaling pathways such as NF-κB, HIF1, and FoxO. Molecular docking showed that 93.3% of the binding activity was less than − 5kcal/mol, indicating good docking affinity. The low-dose of TB significantly reduced the number of coughs in mice within 3 minutes, while the high-dose group showed a significant extension in the latent period of wheezing. The excretion of phenol red in the trachea was significantly increased in the high-dose group. Compared with the normal group, the protein expression levels of TLR4, NF-κB, and MyD88 in the model group were significantly increased (P < 0.001, P < 0.01); compared with the model group, the protein expression levels of TLR4, NF-κB, and MyD88 in the high-dose TB group were significantly decreased (P < 0.01, P < 0.05); compared with the pentosidine group, there were no significant differences among the treatment groups. Conclusions Through experimental verification and network pharmacology analysis, it can be found that TB inhibits the inflammatory response in mice, and its mechanism of action may be related to the inhibition of TLR4/NF-κB signaling pathway activation.