摘要Background:Allergic rhinitis(AR)is a clinical condition with limited effective therapies.Traditional Chinese medicine formulations such as Yupingfeng San(YPFS)demonstrate therapeutic potential for AR.Qifeng Gubiao granules(QFGBG),developed by augmenting YPFS with three additional herbs,have demonstrated immunomodulatory properties and clinical efficacy in AR management.However,the mechanism of QFGBG's anti-AR effects remains unclear.Methods:Chemical components of QFGBG were analyzed using high-performance liquid chromatography.Network pharmacology was employed to predict potential anti-AR targets.A degranulation model was established in rat basophilic leukemia(RBL-2H3)cells stimulated with phorbol 12-myristate-13-acetate and calcium ionophore A23187(PMACI).An AR mouse model was established by intraperitoneal sensitization with ovalbumin(OVA)combined with aluminum hydroxide adjuvant,followed by intranasal administration of OVA.A zebrafish allergy model was induced using compound 48/80(C48/80).The quantification of allergic mediators and inflammatory cytokines was conducted using enzyme-linked immunosorbent assay.The mRNA expression levels of key markers were quantified using qRT-PCR.Additionally,hematoxylin-eosin staining was conducted to evaluate inflammatory infiltration.Western blot assay was utilized to evaluate protein expression levels.Results:QFGBG significantly reduced histamine release,β-hexosaminidase activity,Ca2+influx,and tumor necrosis factor-alpha(TNF-α)levels in PMACI-stimulated RBL-2H3 cells.Network pharmacology analysis revealed that QFGBG may exert therapeutic effects through modulation of the JAK signaling pathway.Furthermore,QFGBG downregulated JAK2 expression while upregulating alpha7 nicotinic acetylcholine receptor(α7nAChR)protein levels.α7nAChR knockdown reversed QFGBG-mediated JAK2 inhibition.Consistent with in vitro results,QFGBG suppressed these inflammatory mediators in both OVA-induced AR mice and C48/80-triggered zebrafish allergy models,while concurrently enhancing α7nAChR mRNA expression.Conclusion:This study demonstrates that QFGBG alleviates AR through α7nAChR-dependent inhibition of mast cell line RBL-2H3 degranulation and inflammatory mediator release via JAK signaling inhibition.These findings enhance the mechanistic understanding of QFGBG in treating allergic disorders while supporting α7nAChR as a therapeutic target for AR intervention.