These results suggested that the anti-inflammatory effects of DHL was associated with the inactivation of NF-κB, and the mechanism of DHL in the protective role in LPS-induced ALI may be that DHL treatment reduced activity of NF-κB mediated by both p38 MAPK/MK2 and Akt signaling pathways, resulted in decreased proinflammatory cytokines in macrophages, and hence suppressed LPS-stimulated lung injury. The gene discussed is AKT1; the disease is acute respiratory distress syndrome.