Baicalin Nasal Irrigation Mitigates Allergic Rhinitis in Mice by Inhibiting Eosinophil Chemotaxis

Introduction Allergic rhinitis (AR) significantly impairs quality of life. Although baicalin is known for its anti-inflammatory properties, its therapeutic potential via localized nasal delivery remains unexplored. This study evaluated the efficacy and potential mechanisms of baicalin nasal irrigation in an AR mouse model. Methods OVA-induced BALB/c mice (n=17 per group) were randomized into six groups: control, AR model, baicalin, loratadine, combination of baicalin and loratadine, and excipient. Nasal symptom scores were recorded pre- and post-treatment. Serum and nasal lavage fluid (NALF) levels of total IgE, OVA-specific IgE, OVA-specific IgG1 and eosinophil cationic protein (ECP) were quantified by ELISA. Nasal mucosal pathology was assessed through hematoxylin and eosin staining (eosinophil counts) and MUC5AC immunofluorescence (goblet cell hyperplasia). Tight junction proteins (ZO-1, occludin) were visualized via immunofluorescence. Transcriptomic profiling of nasal tissues identified baicalin-modulated pathways, with key chemokines validated by immunohistochemistry. Results Baicalin significantly improved nasal symptom scores, reduced eosinophil and goblet cell infiltration, and decreased total IgE, OVA-specific IgE, OVA-specific IgG1, and ECP in serum and NALF. It was more effective than loratadine in reducing tissue eosinophils and suppressing local inflammatory markers. Baicalin also restored mucosal barrier proteins ZO-1 and occludin. Transcriptomic analysis revealed modulation of chemokines (CCL6, CCL8, and CCL24) involved in eosinophil chemotaxis, a finding corroborated by PPI analysis and immunohistochemistry. Conclusion Baicalin nasal irrigation inhibits eosinophil chemotaxis and alleviates AR symptoms, highlighting its potential as a novel local therapeutic strategy for AR.