Objective To study the effect and mechanism of 18β-glycyrrhetinic acid sodium (18β-SGA) on allergic rhinitis (AR) young mice and its improvement on Th1/Th2 imbalance. Methods Fifty young SD rats were randomly divided into control group, model group and 18 groups β SGA low and high dose groups and dexamethasone group, with 10 rats in each group. Except the control group, the other rats established AR model according to ovalbumin sensitization method. The corresponding administration treatment was performed after modeling for 4 weeks. The nasal symptoms of rats were recorded according to the behavioral scoring method. Interleukin-2 (IL-2) and interferon were detected by ELISA-γ （IFN-γ）、The levels of immunoglobulin E (IGE), IL-4 and IL-5. The histopathological changes of rat nasal mucosa were observed by HE staining. The intercellular adhesion molecule 1 (ICAM-1), aquaporin 5 (AQP5) and NF were detected by immunohistochemistry κ Western blot was used to detect NF in nasal mucosa κB and PI3K Akt signaling pathway related proteins were expressed.Results The score of the model group was significantly lower than that of the control group (P=0.002), and there were obvious pathological phenomena such as vasodilation, edema and severe inflammatory cell infiltration in the nasal mucosa. 18 β SGA can alleviate the nasal symptoms of AR in rats， inhibit IL-2 and γ-IFN in serum, increase the contents of IgE, IL-4 and IL-5 （P=0.002，P=0.002）, down regulate ICAM-1, AQP5 and NF in nasal mucosa κ B protein expression (P=0.002; P=0.004; P=0.005), Inhibite P-PI3K, P-Akt and NFκ protein expression of B p65 (P=0.006; P=0.002; P=0.002). Conclusion 18β-SGA can alleviate AR nasal symptoms in rats, and its mechanism may be related to inhibiting the activity of NF-κB and PI3K-Akt signaling pathway and regulating Th1/Th2 balance in vivo.