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Dexmedetomidine Attenuates Neuroinflammatory-Induced Apoptosis after Traumatic Brain Injury via Nrf2 signaling pathway.

F Li | X Wang | Z Zhang | X Zhang | P Gao
Annals of clinical and translational neurology | 2019 Sep

Dexmedetomidine (DEX) exhibits neuroprotective effects as a multifunctional neuroprotective agent in numerous neurological disorders. However, in traumatic brain injury (TBI), the molecular mechanisms of these neuroprotective effects remain unclear. The present study investigated whether DEX, which has been reported to exert protective effects against TBI, could attenuate neuroinflammatory-induced apoptosis and clarified the underlying mechanisms.

Pubmed ID: 31478596

TBI Model

  • Weight-drop model
  • Weight-drop

    • Animal Information

  • Species: rat
  • Strain: Sprague‐Dawley
  • Age (weeks): No age reported
  • Weight (grams): 250 - 280

    • Assessments

    Brain water content, Enzyme‐linked immunosorbent assay, Immunohistochemical, Real‐time quantitative polymerase chain reaction, TUNEL, Terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling, Western blot, neurological severity score

    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

    About

    The PRECISE-TBI toolbox are a collection tools and resources to increase rigor and reproducibility with Traumatic Brain Injury within the PRE Clinical Interagency reSearch resourcE - Traumatic Brain Injury (PRECISE-TBI). Please learn more about PRECISE-TBI at https://www.precise-tbi.org

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    Department of Neurosciences, School of Medicine

    University of California, San Diego





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