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This study aimed to investigate the therapeutic effect of Maiwei Yangfei Decoction(MWYF) on pulmonary fibrosis and its underlying mechanisms. Seventy-two C57BL/6J mice were randomly divided into a blank group, a model group, a low-dose MWYF group, a medium-dose MWYF group, a high-dose MWYF group, and a pirfenidone group. A pulmonary fibrosis model was established by intratracheal instillation of bleomycin. The blank group and the model group were administered double-distilled water daily, while the MWYF groups received corresponding concentrations of MWYF, and the positive control group was given pirfenidone. The severity of pulmonary fibrosis was assessed through Micro-CT scans, histopathological staining of lung tissues, and the expression of collagen Ⅰ and collagen Ⅲ. Network pharmacology combined with transcriptomics analysis was used to explore the anti-fibrotic mechanism of MWYF, which was further validated through in vivo experiments. The results showed that MWYF reduced pulmonary fibrotic lesions, improved inflammation and fibrosis scores, and downregulated the protein expression of collagen Ⅰ and collagen Ⅲ. Network pharmacology and transcriptomics suggested that the anti-fibrotic effect of MWYF was associated with cellular senescence and the p53 signaling pathway. In vivo experiments demonstrated that MWYF significantly reduced senescence-associated β-galactosidase(SA-β-Gal) activity in lung tissues, downregulated the expression of key senescence-related proteins p53, p21, and p16, and decreased cellular senescence, with the high-dose group showing the most pronounced effects. Collectively, these findings demonstrated that MWYF attenuated bleomycin-induced pulmonary fibrosis in mice, likely by suppressing cellular senescence via modulation of the p53 signaling pathway.