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

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 (...

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Bibliographic Details
Published in:Journal of molecular neuroscience 2016-04, Vol.58 (4), p.525-531
Main Authors: Sukumari-Ramesh, Sangeetha, Alleyne, Cargill H.
Format: Article
Language:English
Subjects:
Animals
Antibodies
Antioxidants
Biomedical and Life Sciences
Biomedicine
Brain damage
Cell Biology
Cerebral Hemorrhage - drug therapy
Hematoma
Hemorrhage
Hydroquinones - administration & dosage
Hydroquinones - pharmacology
Hydroquinones - therapeutic use
Interleukins - metabolism
Male
Mice
Microglia - drug effects
Microglia - metabolism
Neurochemistry
Neurology
Neuroprotective Agents - administration & dosage
Neuroprotective Agents - pharmacology
Neuroprotective Agents - therapeutic use
Neurosciences
NF-E2-Related Factor 2 - metabolism
Oxidation
Oxidative stress
Protein Binding
Proteins
Proteomics
Stroke
Transcription factors
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Summary: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.
ISSN:0895-8696
1559-1166
DOI:10.1007/s12031-016-0722-y