Anti-inflammatory Compound MgIG Eases COPD Symptoms in Rat Model

Margarida Maia, PhD avatar

by Margarida Maia, PhD |

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ISM1 | COPD News Today | illustration of animal study

An anti-inflammatory compound used in China to help treat liver disease — known as magnesium isoglycyrrhizinate (MgIG) — eased the symptoms of chronic obstructive pulmonary disease (COPD) by reducing inflammation in the lungs, a study in a rat disease model reported.

“These findings suggest MgIG might be an alternative for COPD therapy,” its scientists wrote.

The study, “Magnesium isoglycyrrhizinate inhibits airway inflammation in rats with chronic obstructive pulmonary disease,” was published in the journal BMC Pulmonary Medicine by a team of researchers at the Jiangsu Vocational College of Medicine in China.

Treatment for COPD usually consists on the use of bronchodilators, corticosteroids, and, when needed, supplemental oxygen and antibiotics.

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However, “as COPD severity increases, all existing drugs get limited to a palliative role,” meaning they are used to relieve symptoms without addressing the cause of the disease.

Researchers thought that a naturally sourced molecule could provide an alternative to existing treatments.

MgIG is a derivative of glycyrrhizic acid extracted from the roots of Chinese liquorice, a flowering plant that is used as a sweetener and in traditional Chinese medicine. As an anti-inflammatory compound, MgIG is also used in that country to help treat hepatitis (liver inflammation) and other inflammatory diseases.

To determine if MgIG could have an anti-inflammatory effect in the lungs, researchers used a rat model of COPD in which the disease is induced by exposing animals to cigarette smoking and lipopolysaccharide, a common antigen found on bacteria.

Rats were either left untreated, or treated with fluticasone plus salmeterol — a combination used as a maintenance treatment for breathing difficulties in COPD — or with MgIG at a low (0.40 mg/kg per day) or high dose (0.80 mg/kg per day). A group of healthy rats served as controls.

The study began with researchers watching for changes in body weight over 1.5 months. While untreated rats lost a considerable amount of weight, those treated with fluticasone plus salmeterol or MgIG were not as affected. Body weight in animals given high-dose MgIG remained closest to control rats.

They next looked at two measures of lung function, forced expiratory volume and forced vital capacity. Both fluticasone plus salmeterol and MgIG protected rats against the declining lung function typically seen in COPD, with high-dose MgIG being almost as effective as fluticasone plus salmeterol.

Further experiments looked more closely at the levels of inflammation in the lungs to understand how MgIG works.

Compared with untreated rats, rats given fluticasone plus salmeterol or MgIG had fewer numbers of white blood cells — immune cells that help the body fight against infections and other diseases — in samples taken from deep within the lungs, indicating less inflammation.

Blood levels of IL-6 and TNF-alpha, two pro-inflammatory cytokines that are known to play a role in COPD progression, were also lower in animals treated with MgIG.

When researchers then took a closer look at lung tissue samples, they saw fewer inflammatory cells, thinner airways, and less mucus production in rats treated with fluticasone plus salmeterol or MgIG than in untreated animals.

At the molecular level, they found that MgIG lowered the levels of NLRP3 and cleaved caspase-1 — two proteins involved in inflammatory response.

“MgIG attenuated pathological [disease] changes in rats with COPD by inhibiting airway inflammation and the NLRP3 signaling pathway,” the researchers wrote, adding that its potential mechanism of action “needs further evaluation.”