Abstract
BackgroundChronic 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.MethodsRat 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.ResultsIt 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.ConclusionIt indicate that MgIG might be an alternative for COPD treatment, and its mechanism of action might be related to the suppression of NLRP3 inflammasome.
Highlights
Chronic obstructive pulmonary disease (COPD) is a kind of chronic lung diseases with the characteristics of airway remodeling and airflow obstruction
Compared with control group (CON) group, FEV0.3/The forced vital capacity (FVC) in model group (MDL) group decreased significantly (P < 0.01), which was reversed in the Salmeterol Fluticasone comparator group (SMF), low dose of MgIG group (LOW) and HIGH group significantly (Fig. 3C–E)
High and low dose of Magnesium isoglycyrrhizinate (MgIG) treatment significantly reversed leukocytes, neutrophils and Monocytes accumulated in bronchoalveolar lavage fluid (BALF) of the COPD rats (P < 0.05 or P < 0.01, Fig. 4A–D)
Summary
Chronic obstructive pulmonary disease (COPD) is a kind of chronic lung diseases with the characteristics of airway remodeling and airflow obstruction. We evaluated the anti-inflammatory effect of MgIG in rats with COPD and investigated the underlying mechanisms. Chronic obstructive pulmonary disease (COPD) is a kind of chronic lung disease characterized by persistent airflow obstruction caused by lung structure destruction, mucus block in airway, and inflammation and swelling. Lung inflammation can cause a considerable increase in leukocytes, lymphocytes (especially C D8+ T cells), neutrophils in different lung compartments [11]. Chronic inflammation of airway and lung is the main driver of the occurrence and development of COPD [14]. Inflammasomes play an important role in the occurrence and development of inflammation in respiratory diseases [15]. NLRP3 might play an important role in chronic inflammation of COPD
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
