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Pretreatment with tert-butylhydroquinone attenuates cerebral oxidative stress in mice after traumatic brain injury.

XY Lu | HD Wang | JG Xu | K Ding | T Li
The Journal of surgical research | 2014 May 01

Traumatic brain injury (TBI) is a worldwide health problem, identified as a major cause of death and disability. Increasing evidence has shown that oxidative stress plays an important role in TBI pathogenesis. The antioxidant transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2), is a known mediator in protection against TBI-induced brain damage. The objective of this study was to test whether tert-butylhydroquinone (tBHQ), a novel Nrf2 activator, can protect against TBI-induced oxidative stress.

Pubmed ID: 24387843

TBI Model

  • Weight-drop model
  • Feeney’s Weight-drop model
  • Animal Information

  • Species: mouse
  • Strain: ICR
  • Age (weeks): No age reported
  • Weight (grams): 28 - 32
  • Assessments

    Brain water content, Enzyme-linked immunosorbent assay (ELISA), Western blot

    TBI model parameters

  • Impact Depth (mm): No information available
  • Impact Duration (ms): No information available
  • Impact Velocity (m/s): No information available
  • Impactor Tip: No information available
  • Device Name

    No information available

    Associated Datasets

    No information available

    Associated Protocols

    No information available