Mechanistic Insights into Qiangjie Xinyi Decoction for Northwest Dryness Syndrome with Allergic Rhinitis: Network Pharmacology and Experimental Validation Methods.

INTRODUCTION: Qiangjie Xinyi Decoction (QJXYD) has been effectively utilized in the clinical treatment of Northwest Dryness Syndrome (NDS) with allergic rhinitis (AR). However, its therapeutic effect lacks a theoretical basis. This study employs network pharmacology and experimental validation to investigate the therapeutic potential of QJXYD on NDS with AR and elucidate its mechanism of action. METHODS: Databases such as TCMSP, OMIM, Genecards, etc. were used to obtain relevant targets for traditional Chinese medicine and diseases. A protein interaction network (PPI) was constructed in the STRING database to screen the core targets of QJXYD for the prevention and treatment of AR. A drug-diseasepathway network diagram was constructed using Cytoscape 3.9.0 to identify the main active ingredients that exert efficacy. Gene Ontology (GO) and KEGG pathway enrichment analyses were performed using the DAVID database. The significant findings were subsequently validated through molecular dynamics simulations. An NDS was established with the AR model in rats, and the network pharmacology results were validated through in vivo experiments. RESULTS: The key targets screened for PPI network construction included IL-6, TNF, VEGFA, etc. Key components such as quercetin, luteolin, and beta-sitosterol were explored in the component target pathway network diagram. GO functional enrichment mainly involved protein binding, inflammatory response, and other functions. KEGG enrichment analysis included pathways such as Th17 cell differentiation and the HIF-1 signaling pathway. Molecular docking and molecular dynamics simulations validated the research results. Animal experiments showed that QJXYD can reduce the protein and gene expression of IL-6, TNF, and VEGFA in the nasal mucosal tissue of NDS with AR rats. DISCUSSION: This study, utilizing network pharmacology and animal experiments, found that QJXYD may target IL-6, TNF, and other targets through components such as quercetin, thereby regulating inflammation-related pathways to treat AR. Animal experiments confirmed that it can reduce the expression of key targets in the nasal mucosa. The research system revealed the mechanism of the compound, but there are limitations, such as unverified predictions and insufficient clinical representativeness of the model, which require further research. CONCLUSION: QJXYD can treat NDS with AR through multiple components, targets, and pathways, providing a theoretical basis for further research.