Magnesium isoglycyrrhizinate inhibits airway inflammation in rats with chronic obstructive pulmonary disease

Abstract 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, whethe...

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Autores principales: Ye Yang, Lei Huang, Chongchong Tian, Bingjun Qian
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Publicado: BMC 2021
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spelling oai:doaj.org-article:4ae236049ccf47f7bb3f09f5c221ef4a2021-11-21T12:39:24ZMagnesium isoglycyrrhizinate inhibits airway inflammation in rats with chronic obstructive pulmonary disease10.1186/s12890-021-01745-71471-2466https://doaj.org/article/4ae236049ccf47f7bb3f09f5c221ef4a2021-11-01T00:00:00Zhttps://doi.org/10.1186/s12890-021-01745-7https://doaj.org/toc/1471-2466Abstract 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.Ye YangLei HuangChongchong TianBingjun QianBMCarticleMgIGCOPDIL-6TNF-αNLRP3 inflammasomeDiseases of the respiratory systemRC705-779ENBMC Pulmonary Medicine, Vol 21, Iss 1, Pp 1-11 (2021)
institution DOAJ
collection DOAJ
language EN
topic MgIG
COPD
IL-6
TNF-α
NLRP3 inflammasome
Diseases of the respiratory system
RC705-779
spellingShingle MgIG
COPD
IL-6
TNF-α
NLRP3 inflammasome
Diseases of the respiratory system
RC705-779
Ye Yang
Lei Huang
Chongchong Tian
Bingjun Qian
Magnesium isoglycyrrhizinate inhibits airway inflammation in rats with chronic obstructive pulmonary disease
description Abstract 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.
format article
author Ye Yang
Lei Huang
Chongchong Tian
Bingjun Qian
author_facet Ye Yang
Lei Huang
Chongchong Tian
Bingjun Qian
author_sort Ye Yang
title Magnesium isoglycyrrhizinate inhibits airway inflammation in rats with chronic obstructive pulmonary disease
title_short Magnesium isoglycyrrhizinate inhibits airway inflammation in rats with chronic obstructive pulmonary disease
title_full Magnesium isoglycyrrhizinate inhibits airway inflammation in rats with chronic obstructive pulmonary disease
title_fullStr Magnesium isoglycyrrhizinate inhibits airway inflammation in rats with chronic obstructive pulmonary disease
title_full_unstemmed Magnesium isoglycyrrhizinate inhibits airway inflammation in rats with chronic obstructive pulmonary disease
title_sort magnesium isoglycyrrhizinate inhibits airway inflammation in rats with chronic obstructive pulmonary disease
publisher BMC
publishDate 2021
url https://doaj.org/article/4ae236049ccf47f7bb3f09f5c221ef4a
work_keys_str_mv AT yeyang magnesiumisoglycyrrhizinateinhibitsairwayinflammationinratswithchronicobstructivepulmonarydisease
AT leihuang magnesiumisoglycyrrhizinateinhibitsairwayinflammationinratswithchronicobstructivepulmonarydisease
AT chongchongtian magnesiumisoglycyrrhizinateinhibitsairwayinflammationinratswithchronicobstructivepulmonarydisease
AT bingjunqian magnesiumisoglycyrrhizinateinhibitsairwayinflammationinratswithchronicobstructivepulmonarydisease
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