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Diabetic pulmonary fibrosis(DPF) is a pulmonary complication of diabetes mellitus with complex pathogenesis, and effective treatments are urgently needed. Buyang Huanwu Decoction(BHD), a potential therapeutic agent for DPF, exhibits hypoglycemic, hypolipidemic, anti-fibrotic, and antioxidative stress effects. In this study, DPF rats were administered BHD via gavage for 3 weeks, and changes in body weight, random blood glucose from tail veins, lipid profiles, oxidative stress markers, and pulmonary collagen deposition were observed. Network pharmacology was employed to analyze the targets and mechanisms of BHD in regulating oxidative stress and lipid metabolism to intervene in DPF. Molecular docking and molecular dynamics simulations were conducted to assess the binding affinity of BHD's active components to core DPF targets, and Western blot was used to detect BHD's regulatory effects on key proteins in DPF rat lungs. The results showed that BHD reduced random blood glucose in DPF rats and alleviated hyperglycemia-induced weight loss, with the moderate-dose group exhibiting the most significant effects, comparable to the metformin group. BHD significantly decreased fasting serum levels of low-density lipoprotein cholesterol, triglycerides, and total cholesterol, enhanced the expression of antioxidative enzymes glutathione peroxidase and superoxide dismutase, and suppressed the oxidative end-product malondialdehyde. HE and Masson staining revealed that BHD intervention restored lung structure, reduced foam cell accumulation, and attenuated collagen deposition. Network pharmacology analysis identified mitogen-activated protein kinase 3(MAPK3), vascular endothelial growth factor A(VEGFA), and prostaglandin-endoperoxide synthase 2(PTGS2) as the primary targets of BHD in modulating oxidative stress and lipid metabolism to intervene in DPF. Enrichment analysis indicated that the advanced glycation end products/receptor for advanced glycation end products(AGE/RAGE) pathway in diabetic complications was the core pathway for BHD's intervention in DPF. Molecular docking demonstrated that astragaloside Ⅳ and baicalein exhibited the strongest binding to PTGS2, while 6-hydroxykaempferol and formononetin showed the strongest binding to MAPK3; molecular dynamics simulations confirmed the stability of these four compound systems. Western blot results indicated that BHD significantly inhibited the activation of phosphorylated extracellular signal-regulated kinase 1/2(p-ERK1/2) and reduced RAGE expression in DPF rat lungs. These findings suggest that BHD may exert anti-DPF effects by inhibiting RAGE, thereby influencing downstream ERK1/2 pathway activation, mitigating oxidative stress, lowering lipid levels, and reducing blood glucose.