| First Author | Wang J | Year | 2007 |
| Journal | Free Radic Biol Med | Volume | 43 |
| Issue | 3 | Pages | 408-14 |
| PubMed ID | 17602956 | Mgi Jnum | J:122813 |
| Mgi Id | MGI:3715560 | Doi | 10.1016/j.freeradbiomed.2007.04.020 |
| Citation | Wang J, et al. (2007) Role of Nrf2 in protection against intracerebral hemorrhage injury in mice. Free Radic Biol Med 43(3):408-14 |
| abstractText | Nrf2 is a key transcriptional factor for antioxidant response element (ARE)-regulated genes. While its beneficial role has been described for stroke, its contribution to intracerebral hemorrhage (ICH)-induced early brain injury remains to be determined. Using wild-type (WT) and Nrf2 knockout (Nrf2(-/-)) mice, the role of Nrf2 in ICH induced by intracerebral injection of collagenase was investigated. The results showed that injury volume was significantly larger in Nrf2(-/-) mice than in WT controls 24 h after induction of ICH (P<0.05), an outcome that correlated with neurological deficits. This exacerbation of brain injury in Nrf2(-/-) mice was also associated with an increase in leukocyte infiltration, production of reactive oxygen species, DNA damage, and cytochrome c release during the critical early phase of the post-ICH period. In combination, these results suggest that Nrf2 reduces ICH-induced early brain injury, possibly by providing protection against leukocyte-mediated free radical oxidative damage. |
