To investigate the potential mechanism of Xiaoqinglong Decoction (XQLD) in treating allergic rhinitis (AR) through autophagy and the IL -33/ST2 pathway.

An ovalbumin (OVA)-sensitized mouse model of allergic rhinitis was established. Twenty-four mice were randomly assigned to four groups: control group, model group, dexamethasone (Dex) group, and XQLD group. All groups except the control received intraperitoneal injections of PBS containing 50 μg OVA and 2 mg aluminum hydroxide on days 1, 7, and 14 for sensitization. From days 21 to 27, mice were challenged intranasally with 400 μg OVA every 24 hours (4 total challenges). Interventions: The XQLD group received XQLD (10. 14 g/kg), the dexamethasone group received dexamethasone disodium phosphate (1 mg/kg), while the model and control groups received equivalent volumes of PBS. All treatments were administered once daily via gavage for 7 days. At 24 h after the final challenge, nasal symptoms (sneezing, scratching, rhinorrhea) were evaluated using a double-blind protocol. Serum was collected for the detection of OVA-specific IgE (OVA-sIgE) and Th1/Th2 cytokines (IL-2, IL-12, IL-5, IL-13) using ELISA. Nasal mucosa tissues underwent Hematoxylin and Eosin (H&E) staining, and immunohistochemical analysis was performed for IL-2, IL-12, IL-5, IL-13, IL-33, ST2, Beclin1, and P62.

compared to the control group, mice in the model group exhibited significantly elevated symptom scores (P < 0.01). The nasal mucosa showed pathological changes including epithelial desquamation, vasodilation, glandular hyperplasia, and extensive inflammatory cell infiltration. Serum OVA-sIgE, IL-5, and IL-13 levels were significantly increased (P < 0.01), while IL-2 and IL-12 levels were decreased (P < 0.01). In nasal mucosa tissue, the protein expression of IL-5, IL-13, IL-33, ST2, and P62 was elevated (P < 0.01), whereas the expression of IL-2, IL-12, and Beclin1 was decreased (P < 0.01). Compared to the model group, mice treated with XQLD and Dex groups showed significantly reduced symptom scores (P < 0.01) and improved nasal mucosal pathology. Serum OVA-sIgE, IL-5, and IL-13 levels decreased (P <0.01), while IL-2 and IL-12 levels increased (P <0.01). In nasal mucosa tissue, the protein expression of IL-2, IL-12, and Beclin1 increased (P <0.01), while the expression of IL-5, IL-13, IL-33, ST2, and P62 decreased (P < 0.01). No statistically significant differences were observed between the XQLD group and the Dex group regarding symptom scores, serum IL-2, IL-12, IL-5, OVA- sIgE levels, and nasal mucosa tissue IL-2, IL-12, IL-5, IL-13, Beclin1, and P62 protein expression (P >0.05).

XQLD alleviates nasal symptoms and pathological damage in AR mice by synergistically regulating Th1/Th2 immune balance through autophagy activation and IL -33/ST2 pathway inhibition.