〔Abstract〕 To explore the active components, key targets, and mechanism of action of turnip in alleviating pulmonary fibrosis (PF) based on network pharmacology and animal experiments. Methods The active components and targets of Brassica rapa L. were screened using the traditional Chinese medicine systems pharmacology database and analysis platform database, and PF-related targets were obtained from disease databases such as online mendelian inheritance of man (OMIM) and DrugBank. The intersection targets were used to construct a protein-protein interaction (PPI) network to identify core targets, followed by gene oncology (GO)/Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis. In the animal experiments, a bleomycin-induced PF mouse model was established. Pathological changes in lung tissue were evaluated using HE and Masson staining. qRT-PCR was used to detect the mRNA expression of tumor necrosis factor-α (TNF-α), phosphatidylinositol 3-kinase (PI3K), and akstrain transforming 1 (AKT1), and immunofluorescence staining was used to measure the protein expression of TNF-α, PI3K, and AKT1. Results The 68 active components identified in Brassica rapa L. may regulate PI3K- Akt signaling pathway by acting on 89 potential targets such as TNF - α and AKT1. The results of animal experiments showed that polysaccharide of Brassica rapa L. (BRPs) could significantly reduce the degree of bleomycin induced pulmonary fibrosis in mice; HE and Masson staining of lung tissue showed that compared with the model group, the damage of alveolar structure, the infiltration of inflammatory cells and the deposition of collagen fibers in the BRPs treatment group were significantly reduced.Further mechanism studies showed that BRPs could significantly down-regulate the mRNA and protein expression levels of TNF-α, PI3K and AKT1 in lung tissue of pulmonary fibrosis mice. Conclusion Brassica rapa L. can synergistically alleviate pulmonary fibrosis through "multi-component, multi-target and multi-channel" approach;BRPs is one of the main active components, and plays an anti-fibrosis role by inhibiting TNF-α/PI3K Akt signaling pathway.