Network pharmacology and experimental validation reveal the multi-target mechanism of Jianpi XiaoxianFormula (BYTQF) against Allergic Rhinitis in mice.

Abstract

To explore the potential active components and mechanisms of Jianpi XiaoxianFormula (BYTQF) in treating allergic rhinitis (AR) using network pharmacology, molecular docking, and experimental validation. Network pharmacology was employed to screen the active components of BYTQF with therapeutic effects on AR. Molecular docking was used to investigate the mechanism of BYTQF in treating AR. Liquid chromatography-mass spectrometry (LC-MS) was applied to identify the chemical components of BYTQF, and a high-performance liquid chromatography (HPLC) method was established for quality control using neochlorogenic acid, chlorogenic acid, and 1,3-dicaffeoylquinic acid as indicators. An AR mouse model was constructed to verify the efficacy of BYTQF through nasal symptom observation and pathological staining. Network pharmacology identified 71 active components in BYTQF, corresponding to 560 targets, while 2193 AR-related targets were retrieved. A total of 186 overlapping targets were obtained. Through PPI network topological analysis, 10 core targets and 10 key components were identified. Molecular docking showed strong binding activity between key components and core targets such as PTGS2 and MMP2. KEGG pathway enrichment analysis revealed significant enrichment of TNF signaling pathway, AGE-RAGE signaling pathway, etc. LC-MS identified 40 chemical components. HPLC analysis of 10 batches of BYTQF showed the contents of neochlorogenic acid, chlorogenic acid, and 1,3-dicaffeoylquinic acid as 0.3147 ± 0.0057 mg/ml, 0.6263 ± 0.0091 mg/ml, and 0.1709 ± 0.0032 mg/ml, respectively. In vivo experiments demonstrated that BYTQF effectively reduced nasal mucosal epithelial thickness and alleviated inflammatory cell infiltration compared to the model group. BYTQF exerts therapeutic effects on AR by inhibiting inflammatory mediators through the interaction of key components (e.g., chlorogenic acid) with core targets (e.g., MMP2) and regulating pathways such as AGE-RAGE, providing a basis for further research and developmentc.