Objective To investigate the effects and mechanism of baicalin in alleviating asthma by regulating the interleukin (IL) -33/ stromal lysin (ST2) signaling pathway.

Methods Asthma mouse models were established, and randomly divided into the model group, low-dose baicalin group (150 mg/kg), high-dose baicalin group (300 mg/kg) and dexamethasone group (1 mg/kg), and normal mice were taken as the control group, with 10 mice in each group. Corresponding drugs were given to each group for intervention. After 4 weeks of intervention, the levels of total serum immunoglobulin (IgE), IL-5 and IL-13 were detected by ELISA. HE and Masson staining were used to observe the pathological changes and collagen precipitation of lung tissue. The proportion of Th1 and Th2 cells in lung tissue was detected by flow cytometry. Immunofluorescence staining and Western blotting were used to detect the protein expressions of IL-33 and ST2 in lung tissue.

Results Compared with the control group, the levels of serum IgE, IL-5, and IL-13, collagen deposition rate in lung tissue, proportion of Th2 cells and protein expressions of IL-33 and ST2 in the model group mice were all increased. However, the proportion of Th1 cells decreased (all P ＜ 0.05). Compared with the model group, the levels of serum IgE, IL-5, and IL-13, rate of collagen deposition in lung tissue, proportion of Th2 cells and protein expressions of IL-33 and ST2 in the low-dose and high-dose baicalin groups and dexamethasone group were all decreased, and the proportion of Th1 cells increased (P ＜ 0.05). The therapeutic effect of baicalin on asthma mice was dose-dependent (P ＜ 0.05), and there was no statistical significance in the protective effects between high-dose baicalin and dexamethasone (P ＞ 0.05).

Conclusions Baicalin can effectively alleviate asthma in mice, restore the Th1/Th2 balance, and improve lung tissue damage and inflammatory responses. Its mechanism of action may be related to the inhibition of the IL-33/ST2 signaling pathway.