Deciphering the pharmacological mechanism of Radix astragali for allergic rhinitis through network pharmacology and experimental validation

• Published in: Scientific reports 2024-12, Vol.14 (1), p.29873-15, Article 29873
• Main Authors: Hua, Yiwei, Tan, Xi, Zhang, Jingwen, Xu, Ningcong, Chen, Ruien, Zhou, Shiqing, Liu, Shaoqing, Li, Kai, Chen, Wenyong, Luo, Qiulan, Li, Yunying
• Format: Article
• Language: English
• Subjects: 631/114; 692/308; 692/699; Allergic rhinitis; Animals; Astragalus propinquus - chemistry; Disease Models, Animal; Drugs, Chinese Herbal - chemistry; Drugs, Chinese Herbal - pharmacology; Hay fever; Humanities and Social Sciences; Humans; Immune response; Inflammation; Male; Mice; Molecular docking and dynamics; Molecular Docking Simulation; multidisciplinary; Network Pharmacology; NF-κB protein; Pharmacology; Physicochemical properties; Phytochemicals; Phytochemicals - chemistry; Phytochemicals - pharmacology; Protein interaction; Protein Interaction Maps - drug effects; Radix astragali; Rhinitis; Rhinitis, Allergic - drug therapy; Rhinitis, Allergic - metabolism; Science; Science (multidisciplinary); Signal Transduction - drug effects; Therapeutic targets; Toll-like receptors
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-024-80101-1

Radix Astragali (RA) has been recognized for its therapeutic potential in allergic rhinitis (AR), yet its potential pharmacological mechanisms remain elusive. This study systematically investigated the physicochemical properties and biological activities of RA’s phytochemicals, aiming to elucidate their targets and mechanisms in AR treatment. We identified 775 potential targets of RA’s key phytochemicals and intersected these with 29,544 AR-related disease targets, pinpointing 747 shared therapeutic targets. A protein-protein interaction network analysis categorized these targets into five subclusters, with TNF, NFKB1, IKBKB, NFKBIA, and CHUK emerging as central nodes. Enrichment analysis revealed their roles in inflammatory and immune responses, particularly through the NF-κB, TNF, IL-17, Toll-like receptor, and NOD-like receptor signaling pathways. Molecular docking and dynamics simulations confirmed the strong binding affinity and stability of RA’s phytochemicals to these targets. In vivo, RA intervention effectively reversed the expression of key inflammatory markers in an IL-13-induced nasal mucosa inflammation model. Our findings suggest that RA’s multitargeted approach involves the modulation of critical inflammatory pathways, highlighting its therapeutic potential.