Exploring the Mechanism of Bufei Decoction in the Treatment of Bronchial Asthma Based on Network Pharmacology and Molecular Docking

Abstract

Background: Bufei decoction (BFD) is used in clinical practice to treat bronchial asthma (BA), although its molecular mechanism of action remains unclear. Objective: This study aimed to explore the molecular mechanism of BFD for treating BA. objective: The aim of this study was to explore the molecular mechanism of BFD for the treatment of BA. Methods: Network pharmacology and molecular docking predicted the molecular mechanism and the analysis results were verified using the ELISA kit and RT-qPCR. method: The molecular mechanism was predicted by the network pharmacology and molecular docking, and the analysis results were verified by ELISA kit and RT-qPCR. Results: There were 58 main active components and 121 potential targets in the BFD from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform( TCMSP), and 11 core targets were obtained from the protein-protein interactions(PPI) network. The gene ontology (GO) analysis found that the treatment of BA with BFD was mainly related to inflammatory reaction, membrane raft, cytokine activity, etc. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showed that it was mainly related to interleukin (IL)-17 signaling pathway, tumor necrosis factor (TNF) signaling pathway, PI3KAkt signaling pathway, etc. The molecular docking results showed that the main active ingredients had strong binding ability with core targets. BFD significantly reduced the TNF-α, IL-6, and IL-1β and increased the level of IL-10 in rats with BA. BFD also significantly reduced the mRNA level of PI3K, AKT1, and VEGFA while increasing the mRNA level of TP53 in rats. result: There were 58 main active components and 121 potential targets in the BFD from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP), and 11 core targets were obtained from protein-protein interactions(PPI) network. The gene ontology (GO) analysis found that the treatment of BA with BFD was mainly related to inflammatory reaction, membrane raft, cytokine activity, etc. The Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analysis showed that it was mainly related to interleukin(IL)-17 signaling pathway, tumor necrosis factor(TNF) signaling pathway, PI3K-Akt signaling pathway ,etc. The results of molecular docking showed that the main active ingredients had strong binding ability with core targets. BFD not only significantly reduced the level of TNF-α, IL-6 and IL-1β but also increased the level of IL-10 in rats with BA. BFD also significantly reduced the mRNA level of PI3K, AKT1 and VEGFA, while increased the mRNA level of TP53 in rats. Conclusion: This study used network pharmacology methods to predict the potential active ingredients, targets, and pathways of BFD in treating BA and explore its possible molecular mechanism, which provided a theoretical basis for further study.