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Ketamine ameliorates oxidative stress-induced apoptosis in experimental traumatic brain injury via the Nrf2 pathway.

J Liang | S Wu | W Xie | H He
Drug design, development and therapy | 2018

Ketamine can act as a multifunctional neuroprotective agent by inhibiting oxidative stress, cellular dysfunction, and apoptosis. Although it has been proven to be effective in various neurologic disorders, the mechanism of the treatment of traumatic brain injury (TBI) is not fully understood. The aim of this study was to investigate the neuroprotective function of ketamine in models of TBI and the potential role of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in this putative protective effect.

Pubmed ID: 29713142

TBI Model

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

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

    Immunohistochemistry (IHC), Nissl staining, Western blot, Brain water content, grip test, spectrophotometer, Neurological Severity Score (NSS)

    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