Magnesium isoglycyrrhizinate alleviate airway inflammatory responses in ovalbumin-induced mouse model of allergic asthma

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.

Keywords:

• MgIG
• inflammation
• asthma
• OVA
• IgE
• NLRP3

Author contributions

YY designed the experiments, finished cells classification and inflammatory factors determination, and wrote the paper; LH finished mouse asthma model construction, immunohistochemistry, and histopathological analysis; CCT finished Western blotting; BJQ analyzed the data and revised the paper.

Disclosure statement

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data availability statement

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Additional information

Funding

The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was supported by the research funding from Jiangsu Provincial Health Commission of China [Z2019053] and Natural Science Foundation of the Jiangsu Higher Education Institutions of China [18KJB320004].