Role of Nrf2 in protection against intracerebral hemorrhage injury in mice

Jian Wang, Jocelyn Fields, Chunying Zhao, John Langer, Rajesh K Thimmulappa, Thomas W. Kensler, Masayuki Yamamoto, Shyam Biswal, Sylvain Doré

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish (US)
Pages (from-to)408-414
Number of pages7
JournalFree Radical Biology and Medicine
Issue number3
StatePublished - Aug 1 2007


  • DNA damage
  • Free radicals
  • Inflammation
  • NF-E2-related factor 2
  • Reactive oxygen species

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)


Dive into the research topics of 'Role of Nrf2 in protection against intracerebral hemorrhage injury in mice'. Together they form a unique fingerprint.

Cite this