Mechanistic Insights into the Anti-COPD 
Effects of an Herbal Extract-based TCM 
Formula, Chuanxing Qingfei Tangjiang, via 
Network Pharmacology and Molecular Docking

Background Chuanxing Qingfei Tangjiang (CQT) is a classic traditional Chinese medicine (TCM) formulation composed of nine herbal components: Mentha haplocalyx (Bohe), Glycyrrhiza uralensis (Gancao), Eriobotrya japonica (Pipaye), Ophiopogon japonicus (Maidong), Prunus armeniaca (Kuxingren), Rehmannia glutinosa (Di huang), Morus alba (Sangye), Platycodon grandiflorus (Jiegeng), and Fritillaria cirrhosa (Chuanbeimu). Traditionally, CQT is used to treat cough, sputum retention, asthma, and chronic obstructive pulmonary disease (COPD). The bioactive compounds extracted from these plants, including flavonoids and alkaloids, are known for their anti-inflammatory and antioxidant properties. Purpose To elucidate the potential molecular mechanisms underlying the anti-COPD effects of CQT through integrated network pharmacology and molecular docking approaches. Materials and Methods Active compounds were identified using the Traditional Chinese Medicine Systems Pharmacology Database and the High-throughput Experiment- and Reference-guided Database of TCM (HERB), and their targets were predicted using SwissTargetPrediction. COPD-related genes were retrieved from GeneCards and Online Mendelian Inheritance in Man. Network construction, Gene Ontology/Kyoto Encyclopedia of Genes and Genomes enrichment, and molecular docking were performed to identify the major pathways and binding interactions. Results A total of 121 bioactive compounds and 221 overlapping COPD-related targets were identified. Key putative pathways involved included the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase-protein kinase B (PI3K-Akt) pathways. Molecular docking demonstrated favorable binding affinities (binding energy < −5 kcal mol–¹, an initial affinity indicator, not a direct measure of biological activity) between major plant-derived compounds (e.g., quercetin, kaempferol, and luteolin) and target proteins (e.g., AKT1, prostaglandin-endoperoxide synthase 2 (PTGS2), and tumor necrosis factor (TNF)). Conclusion This study provides predictive mechanistic insights into how bioactive constituents from CQT may act synergistically to mitigate COPD, supporting further experimental exploration of this herbal formulation as a multi-target natural therapeutic agent. All findings require validation via in vitro (e.g., cell models) and in vivo (e.g., animal models) experiments.