Abstract: The mechanism of Platycodon grandiflorum in the treatment of pulmonary fibrosis was examined by integrated pharmacology network with animal experiment validation. Compositions and targets of Platycodon grandiflorum were collected utilizing databases such as TCMSP and Swiss Target Prediction, whereas pulmonary fibrosis targets were obtained using GeneCards, OMIM, Disgenet, and Drugbank databases. These datasets were merged in order to identify prospective Platycodon grandiflorum targets for the treatment of pulmonary fibrosis. The "drug-component-target-disease" network was constructed with Cytoscape software, and the interaction relationship between potential targets was produced; they were coupled with the String platform to create the PPI network while also doing topological analysis. Then, using R software and the Bioconductor biological information software package, we conduct GO and KEGG enrichment analysis to estimate the therapeutic mechanism. A mouse model of pulmonary fibrosis was constructed for pathological staining, ELISA, lung function, qRT-PCR, and Western blot to validate the results of the network pharmacology. There are 289 putative active components of Platycodon grandiflorum, and 1 129 disease targets for pulmonary fibrosis, for a total of 65 drug-compound-disease common targets. The GO enrichment analysis revealed 1 575 items, whereas the KEGG enrichment analysis yielded 146 entries. The phosphatidylinositol 3 kinase-protein kinase B (PI3K-AKT) signaling pathway, the tumor necrosis factor (TNF) signaling system, and the interleukin-17 (IL-17) signaling pathway were enriched. In animal experiments, Platycodon grandiflorum was found to decrease lung inflammation and collagen deposition in mice with pulmonary fibrosis. According to Western blot results, the expression of PI3K-AKT signaling pathway-related proteins p-PI3K and p-AKT was down-regulated in a dose-dependent manner after Platycodon grandiflorum therapy of pulmonary fibrosis mice. When p-AKT was suppressed, P21 expression was reduced, indicating that Platycodon grandiflorum may control the expression of PI3K-AKT pathway-related proteins to alter cell senescence while treating mice with pulmonary fibrosis. This study uses network pharmacology to identify the targets and pathways of Platycodon grandiflorum against pulmonary fibrosis and conducts related animal experimental validation, providing a foundation for an in-depth discussion of the therapeutic mechanism of Platycodon grandiflorum against pulmonary fibrosis.