Post-Injury Administration of Tert-butylhydroquinone Attenuates Acute Neurological Injury After Intracerebral Hemorrhage in Mice

Sangeetha Sukumari-Ramesh, Cargill H. Alleyne

Research output: Contribution to journalArticle

18 Scopus citations


Intracerebral hemorrhage (ICH) is a severe form of stroke with substantial public health impact. Notably, there is no effective treatment for ICH. Given the role of transcription factor Nrf2 (NF-E2-related factor 2) in antioxidant signaling, herein, we tested the efficacy of tert-butylhydroquinone (TBHQ), a selective inducer of Nrf2 in a preclinical model of ICH. Male CD1 mice were subjected to experimental intracerebral hemorrhage and administered intraperitoneally with TBHQ. The administration of TBHQ enhanced the DNA-binding activity of Nrf2 in the brain and reduced oxidative brain damage in comparison to vehicle-treated ICH. In addition, TBHQ treatment reduced microglial activation with concomitant reduction in the release of proinflammatory cytokine interleukin-1β (IL-1 β). Furthermore, TBHQ treatment attenuated neurodegeneration and improved neurological outcomes after ICH. Altogether, the data demonstrate the efficacy of post-injury administration of TBHQ in attenuating acute neurological injury after ICH.

Original languageEnglish (US)
Pages (from-to)525-531
Number of pages7
JournalJournal of Molecular Neuroscience
Issue number4
Publication statusPublished - Apr 1 2016



  • Gliosis
  • Microglial activation
  • Stroke

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

Cite this