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

178 Citations (Scopus)


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
Pages (from-to)408-414
Number of pages7
JournalFree Radical Biology and Medicine
Issue number3
Publication statusPublished - 2007 Aug 1
Externally publishedYes


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

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)


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