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Study · Animal study (in vivo) · mouse · 2017

14 results

Nicotinamide mononucleotide attenuates brain injury after intracerebral hemorrhage by activating Nrf2/HO-1 signaling pathway.

Wei CC, Kong YY, Li GQ, Guan YF, Wang P, Miao CY

Scientific reports6 Apr 2017Cited by 104 (Europe PMC)

PMID28386082 (opens in a new tab)PMCIDPMC5429727 (opens in a new tab)DOI10.1038/s41598-017-00851-z (opens in a new tab)PepBankPUB-28386082
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Summary

Replenishment of NAD+ has been shown to protect against brain disorders such as amyotrophic lateral sclerosis and ischemic stroke. However, whether this intervention has therapeutic effects in intracerebral hemorrhage (ICH) is unknown. In this study, we sought to determine the potential therapeutic value of replenishment of NAD+ in ICH. In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+. NMN treatment did not decrease hematoma volume and hemoglobin content. However, NMN treatment significantly reduced brain edema, brain cell death, oxidative stress, neuroinflammation, intercellular adhesion molecule-1 expression, microglia activation and neutrophil infiltration in brain hemorrhagic area. Mechanistically, NMN enhanced the expression of two cytoprotective proteins: heme oxygenase 1 (HO-1) and nuclear factor-like 2 (Nrf2). Moreover, NMN increased the nuclear translocation of Nrf2 for its activation. Finally, a prolonged NMN treatment for 7 days markedly promoted the recovery of body weight and neurological function. These results demonstrate that NMN treats brain injury in ICH by suppressing neuroinflammation/oxidative stress. The activation of Nrf2/HO-1 signaling pathway may contribute to the neuroprotection of NMN in ICH.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study14

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice with intracerebral hemorrhage, NMN did not decrease hematoma volume.

    In plain wordsIn mice with brain hemorrhage, NMN did not decrease hematoma volume.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    No significant changeHematoma volume
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · tail veinAs given in this study (mouse).

    Source sentences

    Summary
    NMN treatment did not decrease hematoma volume and hemoglobin content.
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with intracerebral hemorrhage, NMN did not decrease hemoglobin content.

    In plain wordsIn mice with brain hemorrhage, NMN did not decrease hemoglobin content.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    No significant changeHemoglobin content
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · tail veinAs given in this study (mouse).

    Source sentences

    Summary
    NMN treatment did not decrease hematoma volume and hemoglobin content.
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice with intracerebral hemorrhage, NMN significantly reduced brain edema.

    In plain wordsIn mice with brain hemorrhage, NMN reduced brain swelling.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseBrain edema
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · tail veinAs given in this study (mouse).

    Source sentences

    Summary
    However, NMN treatment significantly reduced brain edema, brain cell death, oxidative stress, neuroinflammation, intercellular adhesion molecule-1 expression, microglia activation and neutrophil infiltration in brain hemorrhagic area.
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mice with intracerebral hemorrhage, NMN significantly reduced brain cell death.

    In plain wordsIn mice with brain hemorrhage, NMN reduced brain cell death.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseBrain cell death
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · tail veinAs given in this study (mouse).

    Source sentences

    Summary
    However, NMN treatment significantly reduced brain edema, brain cell death, oxidative stress, neuroinflammation, intercellular adhesion molecule-1 expression, microglia activation and neutrophil infiltration in brain hemorrhagic area.
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mice with intracerebral hemorrhage, NMN significantly reduced oxidative stress in the hemorrhagic brain area.

    In plain wordsIn mice with brain hemorrhage, NMN reduced oxidative stress in the affected brain area.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseOxidative stress
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · tail veinAs given in this study (mouse).

    Source sentences

    Summary
    However, NMN treatment significantly reduced brain edema, brain cell death, oxidative stress, neuroinflammation, intercellular adhesion molecule-1 expression, microglia activation and neutrophil infiltration in brain hemorrhagic area.
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In mice with intracerebral hemorrhage, NMN significantly reduced neuroinflammation.

    In plain wordsIn mice with brain hemorrhage, NMN reduced brain inflammation.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseNeuroinflammation
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated · tail veinAs given in this study (mouse).

    Source sentences

    Summary
    However, NMN treatment significantly reduced brain edema, brain cell death, oxidative stress, neuroinflammation, intercellular adhesion molecule-1 expression, microglia activation and neutrophil infiltration in brain hemorrhagic area.
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In mice with intracerebral hemorrhage, NMN significantly reduced intercellular adhesion molecule-1 expression.

    In plain wordsIn mice with brain hemorrhage, NMN reduced intercellular adhesion molecule-1 expression.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseIntercellular adhesion molecule-1 expression
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated · tail veinAs given in this study (mouse).

    Source sentences

    Summary
    However, NMN treatment significantly reduced brain edema, brain cell death, oxidative stress, neuroinflammation, intercellular adhesion molecule-1 expression, microglia activation and neutrophil infiltration in brain hemorrhagic area.
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In mice with intracerebral hemorrhage, NMN significantly reduced microglia activation.

    In plain wordsIn mice with brain hemorrhage, NMN reduced activation of microglia.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMicroglia activation
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Immune response · Nervous system and cognition
    Studied dose
    Dose not stated · tail veinAs given in this study (mouse).

    Source sentences

    Summary
    However, NMN treatment significantly reduced brain edema, brain cell death, oxidative stress, neuroinflammation, intercellular adhesion molecule-1 expression, microglia activation and neutrophil infiltration in brain hemorrhagic area.
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In mice with intracerebral hemorrhage, NMN significantly reduced neutrophil infiltration in the hemorrhagic brain area.

    In plain wordsIn mice with brain hemorrhage, NMN reduced neutrophil entry into the affected brain area.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseNeutrophil infiltration
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Immune response · Nervous system and cognition
    Studied dose
    Dose not stated · tail veinAs given in this study (mouse).

    Source sentences

    Summary
    However, NMN treatment significantly reduced brain edema, brain cell death, oxidative stress, neuroinflammation, intercellular adhesion molecule-1 expression, microglia activation and neutrophil infiltration in brain hemorrhagic area.
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  10. 10AnimalAnimal study (in vivo)Mechanism

    In mice with intracerebral hemorrhage, NMN enhanced HO-1 expression.

    In plain wordsIn mice with brain hemorrhage, NMN increased HO-1 protein expression.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseHO-1 expression
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated · tail veinAs given in this study (mouse).

    Source sentences

    Summary
    Mechanistically, NMN enhanced the expression of two cytoprotective proteins: heme oxygenase 1 (HO-1) and nuclear factor-like 2 (Nrf2).
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  11. 11AnimalAnimal study (in vivo)Mechanism

    In mice with intracerebral hemorrhage, NMN enhanced Nrf2 expression.

    In plain wordsIn mice with brain hemorrhage, NMN increased Nrf2 protein expression.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseNrf2 expression
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated · tail veinAs given in this study (mouse).

    Source sentences

    Summary
    Mechanistically, NMN enhanced the expression of two cytoprotective proteins: heme oxygenase 1 (HO-1) and nuclear factor-like 2 (Nrf2).
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  12. 12AnimalAnimal study (in vivo)Mechanism

    In mice with intracerebral hemorrhage, NMN increased Nrf2 nuclear translocation.

    In plain wordsIn mice with brain hemorrhage, NMN increased movement of Nrf2 into cell nuclei.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseNrf2 nuclear translocation
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated · tail veinAs given in this study (mouse).

    Source sentences

    Summary
    Moreover, NMN increased the nuclear translocation of Nrf2 for its activation.
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  13. 13AnimalAnimal study (in vivo)Efficacy outcome

    In mice with intracerebral hemorrhage, prolonged NMN treatment promoted body weight recovery.

    In plain wordsIn mice with brain hemorrhage, prolonged NMN treatment improved body weight recovery.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseBody weight recovery
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Body weight · Metabolic and weight
    Studied dose
    Dose not stated · tail vein · 7 daysAs given in this study (mouse).

    Source sentences

    Summary
    Finally, a prolonged NMN treatment for 7 days markedly promoted the recovery of body weight and neurological function.
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.
  14. 14AnimalAnimal study (in vivo)Efficacy outcome

    In mice with intracerebral hemorrhage, prolonged NMN treatment promoted neurological recovery.

    In plain wordsIn mice with brain hemorrhage, prolonged NMN treatment improved recovery of neurological function.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseNeurological recovery
    Study

    mousen: not reported in source

    collagenase-induced intracerebral hemorrhage
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · tail vein · 7 daysAs given in this study (mouse).

    Source sentences

    Summary
    Finally, a prolonged NMN treatment for 7 days markedly promoted the recovery of body weight and neurological function.
    1 context sentence
    Summary · context
    In a collagenase-induced ICH (cICH) mouse model, nicotinamide mononucleotide (NMN), a key intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis, was administrated at 30 minutes post cICH from tail vein to replenish NAD+.

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

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

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