LAUSR

Abstract Objective Asthma is a common chronic airway inflammatory disease, lacking effective therapeutic approaches. Magnesium isoglycyrrhizinate (MgIG) is an anti-inflammatory drug for treating chronic inflammation. However, it is still ambiguous whether MgIG can function in allergy induced asthma. In this study, we investigated the anti-inflammation effect of MgIG in mice with allergy induced asthma and explored the underlying mechanisms. Methods Mouse asthma model was established with ovalbumin (OVA) sensitization and challenge. Subsequently, mice sensitized with OVA were randomly assigned into fourgroups: asthma model group (MDL), dexamethasone group (DXM), MgIG group (MgIG), and normal mice were used as normal control (CON). The mice in MgIG, MDL were given 0.2 mg/mL MgIG solution by atomization inhalation for 30 min before 1% (w/v) OVA challenge. At the completion of model establishment and drug treatment, cells in bronchoalveolar lavage fluid were classified, inflammatory factors in serum were determined, histopathological analysis was performed by H&E staining, and expression of MUC5AC, NLRP3, and cleaved caspase-1 in the lung tissue was also determined by immunohistochemistry and western blotting, respectively. Key findings In comparison to MDL group, MgIG treatment could significantly inhibit the recruitment of white blood cells, neutrophils, and eosinophils in BALF, reduced the production of IL-6, TNF-α, and IgE in serum, and reduced mucus secretion and the infiltration of inflammatory cells. Also, an increase of NLRP3 and Caspase-1 protein levels were suppressed by MgIG treatment. Conclusion Our study findings support that nebulizer inhalation of MgIG as an effective therapy in treating the allergy induced asthma.