Objective To explore the significance of the toxicity mechanism of butyl benzyl phthalate(BBP)in prevention and treatment of pulmonary fibrosis.Methods In this study,we used network toxicology combined with molecular docking technology to screen the targets of BBP and those related to pulmonary fibrosis through PubChem,GeneCards and other databases,and analyzed the intersecting genes by using a Wayne diagram.Protein-protein interaction networks were constructed to screen the core targets,and the pathway mechanisms were revealed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes.Finally,molecular docking using AutoDock was performed to verify the binding patterns of core targets and BBP.Results A total of 91 potential targets of BBP-induced lung fibrosis were screened,among which PTGS2 and CYP3A4 were the core targets(binding energies of-1.84 kcal/mol and-1.68 kcal/mol,respectively).Enrichment analysis showed that BBP regulated the fibrosis process through G protein-coupled receptor signaling pathway,calcium signaling pathway and cyclic adenosine monophosphate signaling pathway.Molecular docking confirmed that BBP was stably bound to the core target through hydrogen bonding and hydrophobic interaction.Conclusion This study provides preliminary insights into the molecular mechanism of BBP-induced pulmonary fibrosis through network toxicology,and PTGS2 and CYP3A4 may play key roles in BBP-induced pulmonary fibrosis,which provides a novel reference for the exploration of the mechanism of toxicant-disease association.

Objective To explore the significance of the toxicity mechanism of butyl benzyl phthalate(BBP)in prevention and treatment of pulmonary fibrosis.Methods In this study,we used network toxicology combined with molecular docking technology to screen the targets of BBP and those related to pulmonary fibrosis through PubChem,GeneCards and other databases,and analyzed the intersecting genes by using a Wayne diagram.Protein-protein interaction networks were constructed to screen the core targets,and the pathway mechanisms were revealed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes.Finally,molecular docking using AutoDock was performed to verify the binding patterns of core targets and BBP.Results A total of 91 potential targets of BBP-induced lung fibrosis were screened,among which PTGS2 and CYP3A4 were the core targets(binding energies of-1.84 kcal/mol and-1.68 kcal/mol,respectively).Enrichment analysis showed that BBP regulated the fibrosis process through G protein-coupled receptor signaling pathway,calcium signaling pathway and cyclic adenosine monophosphate signaling pathway.Molecular docking confirmed that BBP was stably bound to the core target through hydrogen bonding and hydrophobic interaction.Conclusion This study provides preliminary insights into the molecular mechanism of BBP-induced pulmonary fibrosis through network toxicology,and PTGS2 and CYP3A4 may play key roles in BBP-induced pulmonary fibrosis,which provides a novel reference for the exploration of the mechanism of toxicant-disease association.