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Study · Animal study (in vivo) · mouse · 2022

4 results

Nicotinamide Mononucleotide Protects against Retinal Dysfunction in a Murine Model of Carotid Artery Occlusion.

Lee D, Tomita Y, Miwa Y, Jeong H, Shinojima A, Ban N, Yamaguchi S, Nishioka K, Negishi K, Yoshino J, Kurihara T

International journal of molecular sciences25 Nov 2022Cited by 12 (Europe PMC)

PMID36499037 (opens in a new tab)PMCIDPMC9741448 (opens in a new tab)DOI10.3390/ijms232314711 (opens in a new tab)PepBankPUB-36499037
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Summary

Cardiovascular abnormality-mediated retinal ischemia causes severe visual impairment. Retinal ischemia is involved in enormous pathological processes including oxidative stress, reactive gliosis, and retinal functional deficits. Thus, maintaining retinal function by modulating those pathological processes may prevent or protect against vision loss. Over the decades, nicotinamide mononucleotide (NMN), a crucial nicotinamide adenine dinucleotide (NAD+) intermediate, has been nominated as a promising therapeutic target in retinal diseases. Nonetheless, a protective effect of NMN has not been examined in cardiovascular diseases-induced retinal ischemia. In our study, we aimed to investigate its promising effect of NMN in the ischemic retina of a murine model of carotid artery occlusion. After surgical unilateral common carotid artery occlusion (UCCAO) in adult male C57BL/6 mice, NMN (500 mg/kg/day) was intraperitoneally injected to mice every day until the end of experiments. Electroretinography and biomolecular assays were utilized to measure ocular functional and further molecular alterations in the retina. We found that UCCAO-induced retinal dysfunction was suppressed, pathological gliosis was reduced, retinal NAD+ levels were preserved, and the expression of an antioxidant molecule (nuclear factor erythroid-2-related factor 2; Nrf2) was upregulated by consecutive administration of NMN. Our present outcomes first suggest a promising NMN therapy for the suppression of cardiovascular diseases-mediated retinal ischemic dysfunction.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

4 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 carotid artery occlusion, NMN suppressed retinal dysfunction.

    In plain wordsIn mice with carotid artery occlusion, NMN reduced retinal dysfunction.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseRetinal dysfunction
    Study

    mousen: not reported in source

    Male C57BL/6 mice with unilateral common carotid artery occlusion
    Outcome group
    Vision and retina · Eye
    Studied dose
    500 mg/kg/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    We found that UCCAO-induced retinal dysfunction was suppressed, pathological gliosis was reduced, retinal NAD+ levels were preserved, and the expression of an antioxidant molecule (nuclear factor erythroid-2-related factor 2; Nrf2) was upregulated by consecutive administration of NMN.
    2 context sentences
    Summary · context
    After surgical unilateral common carotid artery occlusion (UCCAO) in adult male C57BL/6 mice, NMN (500 mg/kg/day) was intraperitoneally injected to mice every day until the end of experiments.
    Summary · context
    Electroretinography and biomolecular assays were utilized to measure ocular functional and further molecular alterations in the retina.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with carotid artery occlusion, NMN reduced pathological retinal gliosis.

    In plain wordsIn mice with carotid artery occlusion, NMN reduced abnormal retinal gliosis.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreasePathological gliosis
    Study

    mousen: not reported in source

    Male C57BL/6 mice with unilateral common carotid artery occlusion
    Outcome group
    Neuroprotection · Eye
    Studied dose
    500 mg/kg/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    We found that UCCAO-induced retinal dysfunction was suppressed, pathological gliosis was reduced, retinal NAD+ levels were preserved, and the expression of an antioxidant molecule (nuclear factor erythroid-2-related factor 2; Nrf2) was upregulated by consecutive administration of NMN.
    2 context sentences
    Summary · context
    After surgical unilateral common carotid artery occlusion (UCCAO) in adult male C57BL/6 mice, NMN (500 mg/kg/day) was intraperitoneally injected to mice every day until the end of experiments.
    Summary · context
    Electroretinography and biomolecular assays were utilized to measure ocular functional and further molecular alterations in the retina.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mice with carotid artery occlusion, NMN preserved retinal NAD+ levels.

    In plain wordsIn mice with carotid artery occlusion, NMN preserved retinal NAD+ levels.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    Not applicableRetinal NAD+ levels
    Study

    mousen: not reported in source

    Male C57BL/6 mice with unilateral common carotid artery occlusion
    Outcome group
    Receptor activity and mechanism · Eye
    Studied dose
    500 mg/kg/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    We found that UCCAO-induced retinal dysfunction was suppressed, pathological gliosis was reduced, retinal NAD+ levels were preserved, and the expression of an antioxidant molecule (nuclear factor erythroid-2-related factor 2; Nrf2) was upregulated by consecutive administration of NMN.
    2 context sentences
    Summary · context
    After surgical unilateral common carotid artery occlusion (UCCAO) in adult male C57BL/6 mice, NMN (500 mg/kg/day) was intraperitoneally injected to mice every day until the end of experiments.
    Summary · context
    Electroretinography and biomolecular assays were utilized to measure ocular functional and further molecular alterations in the retina.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In mice with carotid artery occlusion, NMN increased retinal Nrf2 expression.

    In plain wordsIn mice with carotid artery occlusion, NMN increased retinal Nrf2 expression.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseNrf2 expression
    Study

    mousen: not reported in source

    Male C57BL/6 mice with unilateral common carotid artery occlusion
    Outcome group
    Receptor activity and mechanism · Eye
    Studied dose
    500 mg/kg/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    We found that UCCAO-induced retinal dysfunction was suppressed, pathological gliosis was reduced, retinal NAD+ levels were preserved, and the expression of an antioxidant molecule (nuclear factor erythroid-2-related factor 2; Nrf2) was upregulated by consecutive administration of NMN.
    2 context sentences
    Summary · context
    After surgical unilateral common carotid artery occlusion (UCCAO) in adult male C57BL/6 mice, NMN (500 mg/kg/day) was intraperitoneally injected to mice every day until the end of experiments.
    Summary · context
    Electroretinography and biomolecular assays were utilized to measure ocular functional and further molecular alterations in the retina.

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

Terms as the source lists them.

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