Mechanisms of Liu Jun Zi Tang in the Treatment of Obstructive Sleep Apnea Hypoventilation Syndrome: Based on a Network Pharmacology Study

Objective To explore the mechanism of Liu-Jun-Zi Tang (LJZT) in treating Obstructive Sleep Apnea Hypoventilation Syndrome (OSAHS) via network pharmacology, molecular docking, and experiments. Methods (1) Active ingredients of LJZT were screened from TCMSP (oral bioavailability OB > 30%, drug-likeness DL > 0.18). (2) Targets of ingredients and OSAHS-related targets were obtained from databases; intersection targets were identified via Venny 2.1. (3) Protein-protein interaction (PPI) network and core targets were analyzed by STRING and Cytoscape. (4) Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment were performed. (5) Molecular docking was validated via AutoDock Tools/Vina. (6) LJZT's chemical composition was analyzed by LC-MS/MS. (7) A hypoxic OSAHS cell model (HUVECs) was used; CCK-8 was screened drug concentration, and ELISA was detected inflammatory factors (IL-6, TNF-α, IL-10), HIF-1α, and pathway proteins (EGFR, SRC, STAT3). Results Nine core ingredients (eg, naringenin) and six core targets (eg, SRC, EGFR) were identified. KEGG enrichment highlighted pathways like HIF-1α signaling. Molecular docking showed favorable binding (binding energy < −4 kcal/mol). LC-MS/MS identified 82 components in LJZT. In hypoxic models, LJZT reduced IL-6, TNF-α, HIF-1α, inhibited EGFR/SRC/STAT3, and increased IL-10 ( P < 0.05). Conclusion LJZT treats OSAHS by regulating the IL-6/EGFR/SRC/STAT3/HIF-1α pathway to alleviate inflammation and hypoxia-induced injury.