SIRT3 regulates bronchial epithelium apoptosis and aggravates airway inflammation in asthma

Sirtuin (SIRT)3 is closely related to inflammation and apoptosis and studies have described this relationship, including in the lungs. However, the expression of SIRT3 and its effect on apoptosis and inflammation in bronchial tissue in asthma remains to be elucidated. The present study found that SIRT3 expression decreased in the bronchial tissues of asthmatic mice and its upregulation could not only reduce increased bronchial epithelial cells apoptosis in the asthmatic mice but also significantly decreased the elevated expression of cytokines (TNF-α, IL-4, IL-5 and IL-13) in bronchoalveolar lavage fluid. Further study found that SIRT3 overexpression significantly decreased apoptosis-related protein expression (Bax/Bcl2 ratio and caspase 3 activity) and oxidative injury. In vitro, SIRT3 regulated oxidative stress-induced bronchial epithelial cell (16HBE) apoptosis and cytokine expression. In conclusion, SIRT3 expression decreased in bronchial tissues of asthmatic mice and the upregulation of SIRT3 expression could reduce the apoptosis of bronchial epithelium and airway inflammation. It was concluded that SIRT3 might be a potential target in asthma treatment.