ArticleFrontiers in cellular and infection microbiology2026
Deciphering the therapeutic mechanisms of Qingfei Litan prescription in acute lung injury: an integrated framework of UHPLC-MS/MS, systems pharmacology, machine learning, and
Article in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Acute lung injury (ALI) is primarily defined by hyper-inflammation and the breakdown of the alveolar-capillary barrier, frequently culminating in refractory respiratory failure. Current clinical interventions-predominantly glucocorticoids and supportive therapies-often yield suboptimal outcomes and are associated with significant side effects. Qingfei Litan Prescription (QFLTP), a traditional Chinese medical prescription indicated for inflammatory respiratory disorders, exhibits significant therapeutic potential; however, the precise molecular mechanisms driving its protective effects are currently under-investigated. Methods: Qualitative detection of the QFLTP ingredients was accomplished via UHPLC-MS/MS analysis. Active ingredients and their potential targets were screened using online prediction tools and traditional Chinese medicine databases, Concurrently, genes associated with ALI were retrieved via GeneCards, DisGeNET, and OMIM repositories. The intersection of these target sets underwent rigorous investigation, encompassing protein-protein interaction (PPI) mapping, alongside Gene Ontology (GO) and KEGG pathway enrichment evaluations, and multiple data-driven algorithms to identify hub genes. Computational modeling and simulation methods were performed to evaluate ligand-target binding. An LPS-induced ALI mouse model was established for Results: A total of 47 chemical constituents and 298 overlapping therapeutic targets were identified. Integrated computational and data-driven analyses highlighted POLB, FGF1, and ARG1 as potential hub genes involved in QFLTP-mediated protection against ALI. GO and KEGG enrichment analyses revealed that pharmacological restorative capacity of QFLTP activity demonstrated a robust functional linkage to inflammatory responses, PI3K-Akt signaling, VEGF signaling, and immune-related pathways. Conclusion: QFLTP exerts protective effects against ALI via its multi-component, multi-target, and multi-pathway mechanisms, potentially by suppressing inflammatory responses, restoring pulmonary barrier integrity, and regulating the expression of hub genes including POLB, FGF1, and ARG1.
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