The present study shows that dietary TA ameliorates CS-induced COPD inflammation by inhibiting inflammatory cytokine release, pathological lung changes (lung injury), and oxidative stress in a dose-dependent manner, and the underlying mechanism of TA treatment for COPD might be mediated by modulation of the AMPK/Nrf2 and NFκB signaling pathways (Figure 7). Here, NFKB1 is linked to chronic obstructive pulmonary disease.