Magnesium isoglycyrrhizinate inhibits airway inflammation in rats with chronic obstructive pulmonary disease
Related Experiment Video
Updated: Oct 13, 2025
Methods for Detecting Cough and Airway Inflammation in Mice
Published on: August 2, 2024
Ye Yang1, Lei Huang1, Chongchong Tian1
1Department of Pharmacology and Medicinal Chemistry, Jiangsu Vocational College of Medicine, Yancheng, 224005, Jiangsu, People's Republic of China.
Background:
Chronic obstructive pulmonary disease (COPD) is a kind of chronic lung diseases with the characteristics of airway remodeling and airflow obstruction. Magnesium isoglycyrrhizinate (MgIG) is an anti-inflammatory glycyrrhizic acid preparation for treating hepatitis. However, whether MgIG can treat other diseases and its action mechanism is still obscure. In this study, we evaluated the anti-inflammatory effect of MgIG in rats with COPD and investigated the underlying mechanisms.
Methods:
Rat model of COPD was constructed by endotracheal-atomized lipopolysaccharide exposure and cigarette smoke induction. Rats were randomly divided into 5 groups: control group, COPD model group, salmeterol fluticasone comparator group, low dose of MgIG group, and high dose of MgIG group. Except for normal control group, the other four groups received sensitization treatment by cigarette smoking and endotracheal-atomization of endotoxin lipopolysaccharide to construct COPD rats model. After model established successfully, the COPD rats in each group received corresponding dose of endotracheal-atomized normal saline, salmeterol fluticasone, and MgIG every day prior to exposure of cigarette smoke from days 30 to 45. Normal control group were treated with normal saline. Finally, All rats were euthanatized. Pulmonary function was measured. Cells in bronchoalveolar lavage fluid were classified, inflammatory factors IL-6 and TNF-α were determined, histopathological analysis was performed by HE staining, and expression of NLRP3 and cleaved caspase-1 in the lung tissue was also determined by Western blotting.
Results:
It showed that MgIG treatment (0.40 or 0.80 mg/kg/day) could recover the weight and the clinical symptoms of rats with COPD, accompanied with lung inflammation infiltration reduction, airway wall attenuation, bronchial mucus secretion reduction. Additionally, MgIG administration reduced inflammatory cells (white blood cells, neutrophils, lymphocytes and monocytes) accumulation in bronchoalveolar lavage fluid and decreased IL-6 and TNF-α production in the serum of COPD rats. Furthermore, MgIG treatment also reduced the expression level of NLRP3 and cleaved caspase-1.
Conclusion:
It indicate that MgIG might be an alternative for COPD treatment, and its mechanism of action might be related to the suppression of NLRP3 inflammasome.
Insights
Magnesium isoglycyrrhizinate (MgIG) effectively treats chronic obstructive pulmonary disease (COPD) in rats by reducing lung inflammation and suppressing the NLRP3 inflammasome pathway. This suggests MgIG could be a novel therapeutic option for COPD patients.
Area of Science:
- Pulmonary Medicine
- Pharmacology
- Immunology
Background:
- Chronic obstructive pulmonary disease (COPD) is characterized by airway remodeling and airflow obstruction.
- Magnesium isoglycyrrhizinate (MgIG), an anti-inflammatory agent, has potential but unconfirmed therapeutic applications beyond hepatitis.
- The precise mechanisms of MgIG in treating inflammatory lung diseases remain largely unexplored.
Purpose of the Study:
- To evaluate the anti-inflammatory effects of MgIG in a rat model of COPD.
- To investigate the underlying molecular mechanisms of MgIG action in COPD.
Main Methods:
- A rat model of COPD was established using lipopolysaccharide and cigarette smoke exposure.
- Rats were treated with varying doses of MgIG, salmeterol fluticasone, or saline.
- Pulmonary function, bronchoalveolar lavage fluid cell counts, inflammatory cytokine levels (IL-6, TNF-α), and NLRP3 inflammasome components were assessed.
Main Results:
- MgIG treatment improved clinical symptoms, reduced lung inflammation, and attenuated airway remodeling in COPD rats.
- MgIG decreased inflammatory cell infiltration and levels of IL-6 and TNF-α in bronchoalveolar lavage fluid and serum.
- MgIG administration downregulated the expression of NLRP3 and cleaved caspase-1.
Conclusions:
- MgIG demonstrates significant anti-inflammatory effects in a rat model of COPD.
- The therapeutic mechanism of MgIG in COPD may involve the suppression of the NLRP3 inflammasome pathway.
- MgIG presents a potential alternative therapeutic agent for COPD treatment.
Related Concept Videos
01:25Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs
Mast cell stabilizers, such as cromolyn (also known as sodium cromoglycate) and nedocromil (Tilade), are effective drugs in asthma management. These stabilizers hinder histamine release by skillfully obstructing the activation of mast cells and other cellular entities. Notably, they navigate this task without...
01:24Antiasthma Drugs: Methylxanthines
Theophylline is thought to inhibit phosphodiesterase enzymes, increasing intracellular levels of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). This rise in cAMP and cGMP concentrations stimulates cardiac function,...
01:20Antiasthma Drugs: Muscarinic Receptor Antagonists
Antimuscarinic agents compete with ACh for the same binding site on the muscarinic receptors. By binding to these receptors, they inhibit the downstream effects of ACh and block the parasympathetic...
01:17Drugs Used in Lower Respiratory Disorders: Overview
Bronchodilators, the first step of respiration enhancement, come in various forms, each with its own mechanism...
01:19Antiasthma Drugs: Leukotriene Modifiers
Leukotriene modifiers work through two distinct mechanisms:
01:26COPD: Management Using Bronchodilators and Corticosteroids