Objective To explore the possible mechanism of the experienced formula Qiyin Sanliangsan（芪银三两三

QYSLS） in the treatment of idiopathic pulmonary fibrosis（IPF）. Methods The TCMSP

GeneCards

NCBI

OMIM databases were searched for active components and action targets of QYSLS and disease targets of IPF; the drug component targets and disease targets were intersected; the STRING database

Cytoscape 3.8.0 software and related plug-ins were used to construct a protein protein interaction（PPI） network; key components were screened; the Database for Annotation

Visualization and Integrated Discovery（DAVID） was used to perform gene ontology（GO） enrichment analysis on core targets

and kyoto encyclopedia of genes and genomes（KEGG） pathway enrichment analysis; the molecular docking technology was used to verify the core target of QYSLS on IPF. Results A total of 147 active components of QYSLS were screened

as well as 664 target points and 1897 IPF-related genes; 141 targets obtained by intersecting drug component targets and IPF disease targets were used to construct a PPI network

and through topology and cluster analysis

STAT3

AKT1

JUN

IL6

MAPK3

SPP1

CASP8

IL1 B

UGT1 A1 and other key targets were gained. GO analysis showed that the action mechanism of QYSLS in the treatment of IPF was involved with the processes such as nutrient induction

oxidative stress

chemical stress

and oxygen perception. The KEGG enrichment pathway was dominated by viral infection-related pathways

inflammation-related pathways and other disease pathways. Molecular docking result showed that the blinding energy of key targets STAT3

AKT1

JUN with quercetin and luteolin was ≤-5.0 Kcal/mol

suggesting good blinding ability. Conclusion The effects of QYSLS on IPF may relate to the action on key targets such as STAT3

AKT1

JUN

and IL6 by regulating signaling pathways related to inflammation

viral infection

cancer and other diseases.