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N-acetylcysteine amide provides neuroprotection via Nrf2-ARE pathway in a mouse model of traumatic brain injury.

Y Zhou | HD Wang | XM Zhou | J Fang | L Zhu | K Ding
Drug design, development and therapy | 2018

Increasing evidence demonstrate N-acetylcysteine amide (NACA) provides neuroprotection and attenuated oxidative stress in rats following traumatic brain injury (TBI). The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) signal pathway is activated after TBI and provides a protective effect against TBI. However, the function and mechanism of NACA in mice after TBI remain unknown. This study was to evaluate the neuroprotection of NACA and the potential action of the Nrf2-ARE pathway in a weight-drop mouse model of TBI.

Pubmed ID: 30584276

TBI Model

  • Weight-drop model
  • Weight-drop

    • Animal Information

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

    • Assessments

    Behavioral, FJC, Immunofluorescence staining, Neurological Severity Score, RT-qPCR, TUNEL, 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

    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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