In summary, our group conducted in vivo and in vitro experiments and showed that MET may upregulate SOD and GSH-Px activities, reduce the oxidation product MDA levels, and downregulate inflammatory factors (TNF-α, IL-1β, and IL-6) by activating the AMPK/NF-κB signaling pathway, thereby participating in the reduction of oxidative damage and the inhibition of inflammation to protect against PQ-induced ALI. The gene discussed is SOD1; the disease is acute respiratory distress syndrome.