Exploring the potential mechanism of Xiaoqinglong Decoction in the treatment of acute exacerbations of chronic obstructive pulmonary disease based on network pharmacology and in silico study

Xiaoqinglong Decoction (XQLD) is a traditional Chinese herbal formula widely used in clinical practice to treat acute exacerbations of chronic obstructive pulmonary disease (AECOPD) with notable efficacy. Studies indicate that XQLD can effectively modulate the inflammatory response during the acute infectious phase of AECOPD; however, its underlying mechanism of action remains unclear. This study employed network pharmacology, molecular docking, and molecular dynamics simulations to investigate the potential target genes of XQLD and its possible mechanisms of action in treating AECOPD. Active ingredients and related targets of XQLD were identified from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform, SwissTargetPrediction, and UniProt. AECOPD-related targets were collected from GeneCards, DrugBank, online Mendelian inheritance in man, and PharmGKB. Common targets between the active ingredients of XQLD and AECOPD were screened. A protein-protein interaction network was constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins database and visualized with Cytoscape. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed using the Database for Annotation, Visualization and Integrated Discovery database. Molecular docking and molecular dynamics simulations were conducted using AutoDock Vina and GROMACS, respectively, to evaluate the binding affinity and stability between core targets and active components. The results revealed that the active ingredients of XQLD, including quercetin, luteolin, and kaempferol, target multiple genes such as nuclear factor kappa B subunit 1, signal transducer and activator of transcription 1, mechanistic target of rapamycin kinase, caspase-3, BCL2‑Like 1, and MYC, primarily through the TNF and PI3K/Akt signaling pathways. Molecular docking and dynamics simulations confirmed stable binding between core targets and active ingredients, particularly between glyuranolide and signal transducer and activator of transcription 1, which merits further investigation. XQLD may alleviate AECOPD progression by regulating the inflammatory response, hypoxia, and apoptosis through multi-component, multi-target, and multi-pathway mechanisms. These findings provide a theoretical basis for further experimental research and potential clinical application of XQLD.