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.
- 1. Department of Neurosurgery, Georgia Regents University, 1120 15th Street, CA1010, Augusta, GA, 30912, USA. [email protected].
- 2. Department of Neurosurgery, Georgia Regents University, 1120 15th Street, CA1010, Augusta, GA, 30912, USA.
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.