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Study · Animal study (in vivo) · rat · 2009

8 results

NNZ-2566, a glypromate analog, improves functional recovery and attenuates apoptosis and inflammation in a rat model of penetrating ballistic-type brain injury.

Lu XC, Chen RW, Yao C, Wei H, Yang X, Liao Z, Dave JR, Tortella FC

Journal of neurotrauma1 Jan 2009Cited by 42 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study8

8 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Safety outcome

    In rats with PBBI, all animals, including NNZ-2566-treated animals, survived 72 h.

    In plain wordsIn rats with brain injury, all animals, including those receiving NNZ-2566, survived 72 h.

    Outcome
    Not applicableSurvival at 72 h
    Study

    ratn: not reported in source

    Penetrating ballistic-type brain injury
    Outcome group
    Mortality · Nervous system and cognition
    Studied dose
    Dose not stated · intravenous · 12 hAs given in this study (rat).

    Source sentences

    Summary
    All animals survived 72 h.
    2 context sentences
    Summary · context
    In this study, we tested NNZ-2566 in a rat model of penetrating ballistic-type brain injury (PBBI) and assessed its effects on injury-induced histopathology, behavioral deficits, and molecular and cellular events associated with inflammation and apoptosis.
    Summary · context
    In the initial dose-response experiments, NNZ-2566 (0.01-3 mg/kg/h x 12 h intravenous infusion) was given at 30 min post-injury and the therapeutic time window was established by delaying treatments 2-4 h post-injury, but with the addition of a 10- or 30-mg/kg bolus dose.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In rats with PBBI, acute NNZ-2566 treatment dose-dependently reduced foot faults by 19-66%.

    In plain wordsIn rats with brain injury, acute NNZ-2566 treatment reduced foot faults.

    Outcome
    DecreaseFoot faults after acute treatment
    Study

    ratn: not reported in source

    Penetrating ballistic-type brain injury
    Outcome group
    Exercise and physical function · Nervous system and cognition
    Studied dose
    0.01-3 mg/kg/h · intravenous · 12 hAs given in this study (rat).

    Source sentences

    Summary
    Behavioral results demonstrated that NNZ-2566 dose-dependently reduced foot faults by 19-66% after acute treatments, and 35-55% after delayed treatments.
    2 context sentences
    Summary · context
    In this study, we tested NNZ-2566 in a rat model of penetrating ballistic-type brain injury (PBBI) and assessed its effects on injury-induced histopathology, behavioral deficits, and molecular and cellular events associated with inflammation and apoptosis.
    Summary · context
    In the initial dose-response experiments, NNZ-2566 (0.01-3 mg/kg/h x 12 h intravenous infusion) was given at 30 min post-injury and the therapeutic time window was established by delaying treatments 2-4 h post-injury, but with the addition of a 10- or 30-mg/kg bolus dose.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In rats with PBBI, delayed NNZ-2566 treatment reduced foot faults by 35-55%.

    In plain wordsIn rats with brain injury, delayed NNZ-2566 treatment reduced foot faults.

    Outcome
    DecreaseFoot faults after delayed treatment
    Study

    ratn: not reported in source

    Penetrating ballistic-type brain injury
    Outcome group
    Exercise and physical function · Nervous system and cognition
    Studied dose
    10- or 30-mg/kg bolus with infusion · intravenous · 12 hAs given in this study (rat).

    Source sentences

    Summary
    Behavioral results demonstrated that NNZ-2566 dose-dependently reduced foot faults by 19-66% after acute treatments, and 35-55% after delayed treatments.
    2 context sentences
    Summary · context
    In this study, we tested NNZ-2566 in a rat model of penetrating ballistic-type brain injury (PBBI) and assessed its effects on injury-induced histopathology, behavioral deficits, and molecular and cellular events associated with inflammation and apoptosis.
    Summary · context
    In the initial dose-response experiments, NNZ-2566 (0.01-3 mg/kg/h x 12 h intravenous infusion) was given at 30 min post-injury and the therapeutic time window was established by delaying treatments 2-4 h post-injury, but with the addition of a 10- or 30-mg/kg bolus dose.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In rats with PBBI, NNZ-2566 did not affect gross lesion volume.

    In plain wordsIn rats with brain injury, NNZ-2566 did not affect gross lesion volume.

    Outcome
    No significant changeGross lesion volume
    Study

    ratn: not reported in source

    Penetrating ballistic-type brain injury
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · intravenous · 12 hAs given in this study (rat).

    Source sentences

    Summary
    Although gross lesion volume was not affected, NNZ-2566 treatment significantly attenuated neutrophil infiltration and reduced the number of activated microglial cells in the peri-lesion regions of the PBBI.
    2 context sentences
    Summary · context
    In this study, we tested NNZ-2566 in a rat model of penetrating ballistic-type brain injury (PBBI) and assessed its effects on injury-induced histopathology, behavioral deficits, and molecular and cellular events associated with inflammation and apoptosis.
    Summary · context
    In the initial dose-response experiments, NNZ-2566 (0.01-3 mg/kg/h x 12 h intravenous infusion) was given at 30 min post-injury and the therapeutic time window was established by delaying treatments 2-4 h post-injury, but with the addition of a 10- or 30-mg/kg bolus dose.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In rats with PBBI, NNZ-2566 significantly attenuated neutrophil infiltration.

    In plain wordsIn rats with brain injury, NNZ-2566 reduced neutrophil infiltration.

    Outcome
    DecreaseNeutrophil infiltration
    Study

    ratn: not reported in source

    Penetrating ballistic-type brain injury
    Outcome group
    Immune response · Nervous system and cognition
    Studied dose
    Dose not stated · intravenous · 12 hAs given in this study (rat).

    Source sentences

    Summary
    Although gross lesion volume was not affected, NNZ-2566 treatment significantly attenuated neutrophil infiltration and reduced the number of activated microglial cells in the peri-lesion regions of the PBBI.
    2 context sentences
    Summary · context
    In this study, we tested NNZ-2566 in a rat model of penetrating ballistic-type brain injury (PBBI) and assessed its effects on injury-induced histopathology, behavioral deficits, and molecular and cellular events associated with inflammation and apoptosis.
    Summary · context
    In the initial dose-response experiments, NNZ-2566 (0.01-3 mg/kg/h x 12 h intravenous infusion) was given at 30 min post-injury and the therapeutic time window was established by delaying treatments 2-4 h post-injury, but with the addition of a 10- or 30-mg/kg bolus dose.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In rats with PBBI, NNZ-2566 reduced activated microglial cells in peri-lesion regions.

    In plain wordsIn rats with brain injury, NNZ-2566 reduced activated microglial cells near the lesion.

    Outcome
    DecreaseActivated microglial cell count
    Study

    ratn: not reported in source

    Penetrating ballistic-type brain injury
    Outcome group
    Immune response · Nervous system and cognition
    Studied dose
    Dose not stated · intravenous · 12 hAs given in this study (rat).

    Source sentences

    Summary
    Although gross lesion volume was not affected, NNZ-2566 treatment significantly attenuated neutrophil infiltration and reduced the number of activated microglial cells in the peri-lesion regions of the PBBI.
    2 context sentences
    Summary · context
    In this study, we tested NNZ-2566 in a rat model of penetrating ballistic-type brain injury (PBBI) and assessed its effects on injury-induced histopathology, behavioral deficits, and molecular and cellular events associated with inflammation and apoptosis.
    Summary · context
    In the initial dose-response experiments, NNZ-2566 (0.01-3 mg/kg/h x 12 h intravenous infusion) was given at 30 min post-injury and the therapeutic time window was established by delaying treatments 2-4 h post-injury, but with the addition of a 10- or 30-mg/kg bolus dose.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In rats with PBBI, NNZ-2566 significantly reversed injury-induced Bax upregulation.

    In plain wordsIn rats with brain injury, NNZ-2566 reduced the injury-related increase in Bax.

    Outcome
    DecreaseBax expression
    Study

    ratn: not reported in source

    Penetrating ballistic-type brain injury
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated · intravenous · 12 hAs given in this study (rat).

    Source sentences

    Summary
    PBBI induced a significant upregulation in Bax expression (36%) and a concomitant downregulation in Bcl-2 expression (33%), both of which were significantly reversed by NNZ-2566.
    2 context sentences
    Summary · context
    In this study, we tested NNZ-2566 in a rat model of penetrating ballistic-type brain injury (PBBI) and assessed its effects on injury-induced histopathology, behavioral deficits, and molecular and cellular events associated with inflammation and apoptosis.
    Summary · context
    In the initial dose-response experiments, NNZ-2566 (0.01-3 mg/kg/h x 12 h intravenous infusion) was given at 30 min post-injury and the therapeutic time window was established by delaying treatments 2-4 h post-injury, but with the addition of a 10- or 30-mg/kg bolus dose.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In rats with PBBI, NNZ-2566 significantly reversed injury-induced Bcl-2 downregulation.

    In plain wordsIn rats with brain injury, NNZ-2566 reversed the injury-related decrease in Bcl-2.

    Outcome
    IncreaseBcl-2 expression
    Study

    ratn: not reported in source

    Penetrating ballistic-type brain injury
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated · intravenous · 12 hAs given in this study (rat).

    Source sentences

    Summary
    PBBI induced a significant upregulation in Bax expression (36%) and a concomitant downregulation in Bcl-2 expression (33%), both of which were significantly reversed by NNZ-2566.
    2 context sentences
    Summary · context
    In this study, we tested NNZ-2566 in a rat model of penetrating ballistic-type brain injury (PBBI) and assessed its effects on injury-induced histopathology, behavioral deficits, and molecular and cellular events associated with inflammation and apoptosis.
    Summary · context
    In the initial dose-response experiments, NNZ-2566 (0.01-3 mg/kg/h x 12 h intravenous infusion) was given at 30 min post-injury and the therapeutic time window was established by delaying treatments 2-4 h post-injury, but with the addition of a 10- or 30-mg/kg bolus dose.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    28 Oct 2026, 02:03 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:37 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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