In lung fibrosis induced by infection with Mycoplasma pneumoniae, NAR reduced autophagy-mediated airway inflammation and lung fibrosis (69, 70), and, in a chronic obstructive pulmonary disease (COPD) model, NAR was able to mitigate lung inflammation, reduce the expression of TGF-β, and increase glucocorticoid receptor expression (GCR) (71). This evidence concerns the gene TGFB1 and chronic obstructive pulmonary disease.