Potential mechanism of Qigebikang tablets in the treatment of allergic rhinitis: Network pharmacology and molecular docking

This study employed network pharmacology and molecular docking to investigate Qige Bi Kang tablets' (QGBK) mechanism against allergic rhinitis (AR). Active ingredients and targets of QGBK were sourced from traditional Chinese medicine systems pharmacology database. AR-related targets were obtained from GeneCards and TTD. The intersection targets were analyzed in STRING for protein-protein interactions, followed by topological analysis in Cytoscape to identify core targets. The R package clusterProfiler performed Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis. AutoDock validated molecular docking between key QGBK ingredients and critical targets. We identified 1174 QGBK active ingredients and 453 AR-related targets. Topological analysis of the protein-protein interaction network yielded 10 core targets. The top 5 targets by degree were signal transducer and activator of transcription (STAT)3, interleukin (IL-6), glyceraldehyde-3-phosphate dehydrogenase, tumor necrosis factor, and nuclear factor-k-gene binding 1. The top 4 key active ingredients by degree were Quercetin, Kaempferol, Emodin, and Palmitic acid. Molecular docking showed binding energies < -3.783 kcal/mol between these molecules and targets, indicating strong affinity. Gene Ontology enrichment revealed QGBK's AR treatment primarily involves responses to polysaccharides, bacterial molecules, xenobiotic stimuli, and positive MAPK cascade regulation. Kyoto Encyclopedia of Genes and Genomes analysis highlighted the AGE-RAGE and IL-17 signaling pathways as significant. In conclusion, QGBK's anti-AR mechanism exhibits multicomponent, multi-target, multi-pathway regulation. Quercetin, Kaempferol, Emodin, and Palmitic acid are key therapeutic components, acting on core targets like STAT3, IL-6, glyceraldehyde-3-phosphate dehydrogenase, and MMP9. QGBK exerts its effects through triple mechanisms: anti-inflammation, immunomodulation, and mitigation of airway responsiveness, primarily via STAT3/IL-6 signaling modulation. However, further in vivo and clinical validation is essential. Future research should prioritize unlocking QGBK's clinical translation potential and advancing targeted formulation development.