Peripheral administration of a novel diketopiperazine, NNZ 2591, prevents brain injury and improves somatosensory-motor function following hypoxia-ischemia in adult rats.

Guan J, Mathai S, Harris P, Wen JY, Zhang R, Brimble M, Gluckman P

Neuropharmacology19 Aug 2007Cited by 38 (Europe PMC)

PMID17904590DOI10.1016/j.neuropharm.2007.08.010PepBankPUB-17904590

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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 study13

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

01AnimalAnimal study (in vivo)Efficacy outcome
In rats with hypoxic-ischemic injury, central NNZ‑2591 reduced lateral cortical brain damage.
In plain wordsIn rats with hypoxic-ischemic injury, central NNZ‑2591 reduced lateral cortical brain damage.
Peptide
NNZ-2591
Outcome
DecreaseLateral cortex brain damage
Study
ratsn: not reported in source
hypoxic-ischemic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated · intracerebroventricularAs given in this study (rats).
Source sentences
Summary
Central administration of cyclic GP or NNZ 2591 reduced the extent of brain damage in the lateral cortex, the hippocampus and the striatum (p<0.001), with NNZ 2591 being more potent.
2 context sentences(design, population, supporting numbers)
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459001
02AnimalAnimal study (in vivo)Efficacy outcome
In rats with hypoxic-ischemic injury, central NNZ‑2591 reduced hippocampal brain damage.
In plain wordsIn rats with hypoxic-ischemic injury, central NNZ‑2591 reduced hippocampal brain damage.
Peptide
NNZ-2591
Outcome
DecreaseHippocampal brain damage
Study
ratsn: not reported in source
hypoxic-ischemic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated · intracerebroventricularAs given in this study (rats).
Source sentences
Summary
Central administration of cyclic GP or NNZ 2591 reduced the extent of brain damage in the lateral cortex, the hippocampus and the striatum (p<0.001), with NNZ 2591 being more potent.
2 context sentences(design, population, supporting numbers)
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459002
03AnimalAnimal study (in vivo)Efficacy outcome
In rats with hypoxic-ischemic injury, central NNZ‑2591 reduced striatal brain damage.
In plain wordsIn rats with hypoxic-ischemic injury, central NNZ‑2591 reduced striatal brain damage.
Peptide
NNZ-2591
Outcome
DecreaseStriatal brain damage
Study
ratsn: not reported in source
hypoxic-ischemic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated · intracerebroventricularAs given in this study (rats).
Source sentences
Summary
Central administration of cyclic GP or NNZ 2591 reduced the extent of brain damage in the lateral cortex, the hippocampus and the striatum (p<0.001), with NNZ 2591 being more potent.
2 context sentences(design, population, supporting numbers)
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459003
04AnimalAnimal study (in vivo)Efficacy outcome
In rats with hypoxic-ischemic injury, central NNZ‑2591 was more potent than cyclic GP in reducing brain damage.
In plain wordsIn rats with hypoxic-ischemic injury, central NNZ‑2591 reduced brain damage more potently than cyclic GP.
Peptide
NNZ-2591
Outcome
IncreaseNeuroprotective potency versus cyclic GP
Study
ratsn: not reported in source
hypoxic-ischemic brain injury
Comparator
Cyclic GP
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated · intracerebroventricularAs given in this study (rats).
Source sentences
Summary
Central administration of cyclic GP or NNZ 2591 reduced the extent of brain damage in the lateral cortex, the hippocampus and the striatum (p<0.001), with NNZ 2591 being more potent.
2 context sentences(design, population, supporting numbers)
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459004
05AnimalAnimal study (in vivo)Pharmacokinetics
In rats, NNZ‑2591 was stable in plasma.
In plain wordsIn rats, NNZ‑2591 remained stable in plasma.
Peptide
NNZ-2591
Outcome
Not applicablePlasma stability
Study
ratsn: not reported in source
normal and hypoxic-ischemic injured rats
Outcome group
Pharmacokinetics · Pharmacology
Studied dose
Dose not stated
Source sentences
Summary
NNZ 2591 was stable in the plasma and crossed the blood-brain barrier independent of hypoxic-ischemic injury.
3 context sentences(design, population, supporting numbers)
Summary · context
The central uptake of NNZ 2591 was also examined in normal and hypoxic-ischemic injured rats by HPLC-mass spectrometry.
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459005
06AnimalAnimal study (in vivo)Pharmacokinetics
In rats, NNZ‑2591 crossed the blood-brain barrier independently of hypoxic-ischemic injury.
In plain wordsIn rats, NNZ‑2591 crossed the blood-brain barrier with or without hypoxic-ischemic injury.
Peptide
NNZ-2591
Outcome
Not applicableBlood-brain barrier crossing
Study
ratsn: not reported in source
normal and hypoxic-ischemic injured rats
Outcome group
Pharmacokinetics · Pharmacology
Studied dose
Dose not stated
Source sentences
Summary
NNZ 2591 was stable in the plasma and crossed the blood-brain barrier independent of hypoxic-ischemic injury.
3 context sentences(design, population, supporting numbers)
Summary · context
The central uptake of NNZ 2591 was also examined in normal and hypoxic-ischemic injured rats by HPLC-mass spectrometry.
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459006
07AnimalAnimal study (in vivo)Pharmacokinetics
In rats, CSF NNZ‑2591 levels persisted for 2 h after a single subcutaneous dose.
In plain wordsIn rats, NNZ‑2591 levels in spinal fluid persisted for 2 h after a single subcutaneous dose.
Peptide
NNZ-2591
Outcome
Not applicableCSF persistence
Study
ratsn: not reported in source
hypoxic-ischemic brain injury
Outcome group
Pharmacokinetics · Pharmacology
Studied dose
Dose not stated · subcutaneousAs given in this study (rats).
Source sentences
Summary
The level of NNZ 2591 in the CSF was maintained for 2 h after a single subcutaneous dose,
2 context sentences(design, population, supporting numbers)
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459007
08AnimalAnimal study (in vivo)Efficacy outcome
In rats with hypoxic-ischemic injury, bolus subcutaneous NNZ‑2591 produced modest neuroprotection.
In plain wordsIn rats with hypoxic-ischemic injury, a subcutaneous NNZ‑2591 dose produced modest brain protection.
Peptide
NNZ-2591
Outcome
IncreaseNeuroprotection after subcutaneous bolus
Study
ratsn: not reported in source
hypoxic-ischemic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated · subcutaneousAs given in this study (rats).
Source sentences
Summary
The level of NNZ 2591 in the CSF was maintained for 2 h after a single subcutaneous dose, and modest neuroprotection was seen after a bolus subcutaneous administration (overall p<0.001).
2 context sentences(design, population, supporting numbers)
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459008
09AnimalAnimal study (in vivo)Efficacy outcome
In rats with hypoxic-ischemic injury, subcutaneous NNZ‑2591 improved somatosensory-motor function.
In plain wordsIn rats with hypoxic-ischemic injury, subcutaneous NNZ‑2591 improved sensory and motor function.
Peptide
NNZ-2591
Outcome
IncreaseSomatosensory-motor function
Study
ratsn: not reported in source
hypoxic-ischemic brain injury
Outcome group
Exercise and physical function · Nervous system and cognition
Studied dose
Dose not stated · subcutaneous · 5 dAs given in this study (rats).
Source sentences
Summary
Treatment with NNZ 2591 for 5 d subcutaneously improved somatosensory-motor function (p<0.05) and long-term histological outcome (overall p<0.0001).
2 context sentences(design, population, supporting numbers)
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459009
10AnimalAnimal study (in vivo)Efficacy outcome
In rats with hypoxic-ischemic injury, subcutaneous NNZ‑2591 improved long-term histological outcome.
In plain wordsIn rats with hypoxic-ischemic injury, subcutaneous NNZ‑2591 improved long-term tissue outcomes.
Peptide
NNZ-2591
Outcome
IncreaseLong-term histological outcome
Study
ratsn: not reported in source
hypoxic-ischemic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated · subcutaneous · 5 dAs given in this study (rats).
Source sentences
Summary
Treatment with NNZ 2591 for 5 d subcutaneously improved somatosensory-motor function (p<0.05) and long-term histological outcome (overall p<0.0001).
2 context sentences(design, population, supporting numbers)
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459010
11AnimalAnimal study (in vivo)Mechanism
In rats with hypoxic-ischemic injury, NNZ‑2591 reduced caspase-3-mediated apoptosis.
In plain wordsIn rats with hypoxic-ischemic injury, NNZ‑2591 reduced caspase-3-mediated cell death.
Peptide
NNZ-2591
Outcome
DecreaseCaspase-3-mediated apoptosis
Study
ratsn: not reported in source
hypoxic-ischemic brain injury
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
NNZ 2591 treatment not only reduced both caspase-3 mediated apoptosis and microglial activation but also enhanced astrocytic reactivity, which may mediate its protective effect.
2 context sentences(design, population, supporting numbers)
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459011
12AnimalAnimal study (in vivo)Mechanism
In rats with hypoxic-ischemic injury, NNZ‑2591 reduced microglial activation.
In plain wordsIn rats with hypoxic-ischemic injury, NNZ‑2591 reduced microglial activation.
Peptide
NNZ-2591
Outcome
DecreaseMicroglial activation
Study
ratsn: not reported in source
hypoxic-ischemic brain injury
Outcome group
Inflammation markers · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
NNZ 2591 treatment not only reduced both caspase-3 mediated apoptosis and microglial activation but also enhanced astrocytic reactivity, which may mediate its protective effect.
2 context sentences(design, population, supporting numbers)
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459012
13AnimalAnimal study (in vivo)Mechanism
In rats with hypoxic-ischemic injury, NNZ‑2591 enhanced astrocytic reactivity.
In plain wordsIn rats with hypoxic-ischemic injury, NNZ‑2591 increased astrocyte reactivity.
Peptide
NNZ-2591
Outcome
IncreaseAstrocytic reactivity
Study
ratsn: not reported in source
hypoxic-ischemic brain injury
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
NNZ 2591 treatment not only reduced both caspase-3 mediated apoptosis and microglial activation but also enhanced astrocytic reactivity, which may mediate its protective effect.
2 context sentences(design, population, supporting numbers)
Summary · context
The compounds were given either intracerebroventricularly or subcutaneously 2h after hypoxia-ischemia.
Summary · context
Histology, immunohistochemistry and behavior were used to evaluate treatment effects.
Report a problemFND-1790459013

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.

Version 2Current
27 Oct 2026, 18:20 UTC
Study results updated
Version 1
27 Oct 2026, 16:32 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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