1. Academic Validation
  2. Post-Injury Administration of Tert-butylhydroquinone Attenuates Acute Neurological Injury After Intracerebral Hemorrhage in Mice

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

  • J Mol Neurosci. 2016 Apr;58(4):525-31. doi: 10.1007/s12031-016-0722-y.
Sangeetha Sukumari-Ramesh 1 Cargill H Alleyne Jr 2
Affiliations

Affiliations

  • 1 Department of Neurosurgery, Georgia Regents University, 1120 15th Street, CA1010, Augusta, GA, 30912, USA. sramesh@gru.edu.
  • 2 Department of Neurosurgery, Georgia Regents University, 1120 15th Street, CA1010, Augusta, GA, 30912, USA.
Abstract

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.

Keywords

Gliosis; Microglial activation; Stroke.

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