Fig. 4

Trx prevents and relieves COPD pathogenesis through multiple molecular mechanisms. Trx eliminates MIF to improve glucocorticoid resistance and eliminates ROS and inhibits neutrophil infiltration by regulating adhesion molecules to suppress the production of cytokines to reduce oxidative stress and inflammation. Trx exerts its anti-oxidative and anti-inflammatory effects by regulating the NF-κB, MAPK, PI3K/Akt and cAMP-PKA pathways. Trx also inhibits the airway neutrophil recruitment by down-regulating the expression of neutrophil L-selectin on circulating neutrophils. Trx is subtle in regulating the balance between protease and antiprotease. Trx has inhibitory effect on both, but it is asymmetric in its inhibition. Trx has stronger inhibitory effects on over-generated proteases, thus maintaining the balance of the protease–antiprotease system. Moreover, Trx down-regulates the expression of EGFR and TGF in the airway to reduce mucus secretion, airway remodelling and pulmonary fibrosis