PM2.5 inhibits SOD1 expression by up-regulating microRNA-206 and promotes ROS accumulation and disease progression in asthmatic mice

Bronchial asthma is the most common chronic respiratory disease. Chronic airway inflammation, airflow restriction and airway hyper-responsiveness are its main manifestations. In recent decades, the prevalence and mortality of asthma have been increasing all over the world, which seriously threatens public health. Research suggests that air pollution is associated with the increased incidence of asthma. PM2.5 is one of the most complex pollutants in the atmospheric environment and harmful to human health. It is related to the incidence of asthma. However, the molecular mechanism of PM2.5 in the development of asthma is still unclear. In this study, we established a mouse model of asthma using CRE to observe the effect of PM2.5 on the symptoms of asthmatic mice and its possible molecular mechanism. The results showed that PM2.5 could significantly increase airway resistance and pulmonary inflammation, increase the number of inflammatory cells, eosinophils, macrophages, neutrophils and lymphocytes in bronchoalveolar lavage fluid in asthmatic mice. Moreover, PM2.5 could reduce the contents of antioxidant enzymes such as CAT, GSH, GSH-Px and T-SOD in lung tissue of mice, and increase the ROS level. PM2.5 can promote the expression of microRNA-206 in lung tissue of mice. miR-206 can target the 3'-UTR of SOD1 to inhibit SOD1 expression, which leads to the increase of ROS level and aggravates pulmonary inflammatory response and asthma symptoms in asthmatic mice. This study found the possible molecular mechanism of PM2.5 aggravating asthma, and miR-206 may be a potential target for asthma treatment.