This occurs through activating downstream antioxidant enzymes, such as HO-1, superoxide dismutase (SOD), and NADPH quinone oxidoreductase 1 (NQO1).52 Recently, Hu et al. reported that Nrf2-knockout exacerbates HIE phenotypes in mice.53 Further analysis showed that Nrf2 activation attenuates inflammation and oxidative stress in HI-induced brain injury.54 Our findings here are consistent with these reports and reveal that Cel treatment increased levels of Nrf2 protein and a downstream target HO-1 in neonatal HI rats. This evidence concerns the gene HMOX1 and injury.