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This study systematically revealed the inflammatory mechanism of action of the Qibai Pingfei Capsules in intervening in phlegm-stasis obstructing lung syndrome in chronic obstructive pulmonary disease(COPD) based on network pharmacology, molecular docking, molecular dynamics simulation, and experimental validation. Core components such as kaempferol and inosine, as well as key targets such as hypoxia-inducible factor-1α(HIF-1α) and prostaglandin-endoperoxide synthase 2(PTGS2)/cyclooxygenase-2(COX-2), were identified via network pharmacology, and a multidimensional interaction network was constructed. Enrichment analysis suggested that these core targets may exert regulatory effects by modulating biological processes such as hypoxic stress response, inflammatory mediator release, and angiogenesis, with potential mechanisms related to the regulation of inflammation-related signaling pathways. Molecular dynamics simulations confirmed that the key components stably bound to targets such as HIF-1α, COX-2, and tumor necrosis factor-α(TNF-α). A rat model of COPD with phlegm-stasis obstructing lung syndrome was established using a composite stimulation method(hypoxia + swimming + cigarette smoke). The results demonstrated that Qibai Pingfei Capsules could significantly improve lung function, as evidenced by increased lung function parameters(FVC, FEV_(0.3), FEV_(0.3)/FVC), and reduced inflammatory cell infiltration in lung tissue. Pathological damage to bronchi and alveolar structures in the Qibai Pingfei Capsules group was significantly alleviated, characterized by reduced airway remodeling and thinning of alveolar septa. Qibai Pingfei Capsules inhibited the expression of HIF-1α and COX-2 proteins(P<0.01) and significantly downregulated the level of the pro-inflammatory factor TNF-α. Co-immunoprecipitation confirmed the interaction between HIF-1α and COX-2 proteins in rat lung tissue. In-depth analysis revealed that the therapeutic mechanism of Qibai Pingfei Capsules may involve targeting and regulating the HIF-1α/COX-2 signaling pathway to intervene in the hypoxic stress response, thereby modulating TNF-α-mediated inflammatory cascades. This mechanism effectively modulated hypoxic stress and the inflammatory microenvironment, promoted lung tissue repair, and significantly reduced pulmonary inflammation levels in the rat model of COPD with phlegm-stasis obstructing the lung syndrome.