In the current study, we have demonstrated that up-regulation of HO-1 by its activator hemin, through reducing NF-κB p65 activation and enhancing Nrf2, reduced lung oxidative stress (by increasing SOD activities and reducing MDA, H2O2) and inflammation (by decreasing TNF-α, IL-6, and MPO), and subsequently attenuated OALT-induced ALI and finally increased the survival rate of rats. The gene discussed is NFKB1; the disease is acute respiratory distress syndrome.