Objective To observe the inhibitory effect of deguelin on allergic asthma in young rats and to explore its mechanism of action. Methods Fifty 4-weeks-old SPF BALB/c mice were randomly divided into normal group, model group, methylprednisolone group, deguelin high-dose group, deguelin low-dose group, 10 mice in each group. Except for the normal group, mice in all other groups were sensitized and stimulated by ovalbumin (OVA) to establish an allergic asthma model. Dosing started on the 21st day of modeling. 1 h before atomization, the mice in the high-dose deguelin group and low-dose deguelin group were intraperitoneally injected with 4 mg/kg and 2 mg/kg deguelin, respectively. The mice in methylprednisolone group were intraperitoneally injected with 10 mg/kg methylprednisolone injection, and the mice in the normal group and model group were intraperitoneally injected with the same amount of normal saline once a day for 3 consecutive days. The mice plasma and bronchoalveolar lavage fluid (BALF) were collected. ELISA kits was used to detect plasma total IgE and BALF IL-1β and IL-13 levels in BALF. HE staining was used to observe the pathological changes of lung tissues in mice. qRT-PCR was used to detect IL-1β and IL-13 mRNA levels in mice lung tissues. Western blot was used to detect lung tissues p NF-κB p65, p-IκBα, p-p38 MAPK, p -ERK1/2, p-JNK protein expression levels. Results Compared with the normal group, the plasma IgE level of the model group and the IL-1β, IL-13 content and mRNA expression in BALF were significantly increased (P＜0.05). The total number of inflammatory cells, neutrophils, eosinophils and lymphocytes in the BALF were higher than the normal group. Compared with the model group, high and low dose deguelin could reduce the level of plasma IgE and the content and mRNA expression of IL-1 β, IL-13 in BALF, and the total number of inflammatory cells, neutrophils, eosinophils and lymphocytes in BALF were decreased (P＜0.05). There was no significant difference in BALF inflammatory cell count between deguelin high-dose group and methylprednisolone group (P＞0.05). HE staining results showed that there was no inflammatory cell infiltration in the lung tissues of the normal group. Compared with the normal group, the inflammatory cell infiltration in the lung tissues of the model group were obvious, and the alveolar wall were abnormally thickened. Compared with the model group, the inflammatory cell infiltration and alveolar wall edema and thickening around the airway vessels of mice in the high and low doses of deguelin were reduced. Western blot results showed that compared with the normal group, the expression levels of p-NF-κB p65, p-IκBα, p-p38 MAPK, p-ERK1/2, and p-JNK protein in the lung tissues of the model group were significantly increased (P＜0.05). Compared with the model group, the protein expression of p-NF-κB p65, p-IκBα, p-p38 MAPK, p-ERK1/2, and p-JNK protein were decreased in the high-dose and low-dose deguelin groups (P＜0.05). The protein expression levels of p-NF-κB p65, p-IκBα, pp38 MAPK, p-ERK1/2, and p-JNK protein in deguelin high-dose group were not significantly different from those in methylprednisolone group (P＞0.05). Conclusion Deguelin can improve allergic asthma in young rats, and its mechanism is related to the inhibition of the activation of NF-κB/MAPK signaling pathway.