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Study · In vitro (cells) · rat · 2008

8 results

Cellular NAD replenishment confers marked neuroprotection against ischemic cell death: role of enhanced DNA repair.

Wang S, Xing Z, Vosler PS, Yin H, Li W, Zhang F, Signore AP, Stetler RA, Gao Y, Chen J

Stroke10 Jul 2008Cited by 103 (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

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In rat neuronal cultures, NAD(+) repletion before or after oxygen-glucose deprivation reduced cell death in a concentration- and time-dependent manner.

    In plain wordsIn cells from rats, NAD(+) repletion reduced cell death compared with cultures without NAD(+) repletion.

    Outcome
    DecreaseCell death
    Study

    ratn: not reported in source

    Primary neuronal cultures exposed to oxygen-glucose deprivation
    Comparator
    Without NAD(+) repletion
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Direct NAD(+) repletion in neurons either before or after OGD markedly reduced cell death and OGD-induced accumulation of DNA damage (AP sites, single and double strand breaks) in a concentration- and time-dependent manner.
    3 context sentences
    Summary · context
    In vitro ischemic injury was induced in rat primary neuronal cultures by oxygen-glucose deprivation (OGD) for 1 to 2 hours.
    Summary · context
    NAD(+) was replenished by adding NAD(+) directly to the culture medium before or after OGD.
    Summary · context
    Cell viability, oxidative DNA damage, and DNA base-excision repair (BER) activity were measured quantitatively up to 72 hours after OGD with or without NAD(+) repletion.
  2. 02LabIn vitro (cells)Mechanism

    In rat neuronal cultures, NAD(+) repletion reduced oxygen-glucose deprivation-induced AP site accumulation.

    In plain wordsIn cells from rats, NAD(+) repletion reduced AP site accumulation compared with cultures without NAD(+) repletion.

    Outcome
    DecreaseAP site accumulation
    Study

    ratn: not reported in source

    Primary neuronal cultures exposed to oxygen-glucose deprivation
    Comparator
    Without NAD(+) repletion
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Direct NAD(+) repletion in neurons either before or after OGD markedly reduced cell death and OGD-induced accumulation of DNA damage (AP sites, single and double strand breaks) in a concentration- and time-dependent manner.
    3 context sentences
    Summary · context
    In vitro ischemic injury was induced in rat primary neuronal cultures by oxygen-glucose deprivation (OGD) for 1 to 2 hours.
    Summary · context
    NAD(+) was replenished by adding NAD(+) directly to the culture medium before or after OGD.
    Summary · context
    Cell viability, oxidative DNA damage, and DNA base-excision repair (BER) activity were measured quantitatively up to 72 hours after OGD with or without NAD(+) repletion.
  3. 03LabIn vitro (cells)Mechanism

    In rat neuronal cultures, NAD(+) repletion reduced oxygen-glucose deprivation-induced single-strand DNA breaks.

    In plain wordsIn cells from rats, NAD(+) repletion reduced single-strand DNA breaks compared with cultures without NAD(+) repletion.

    Outcome
    DecreaseSingle-strand DNA breaks
    Study

    ratn: not reported in source

    Primary neuronal cultures exposed to oxygen-glucose deprivation
    Comparator
    Without NAD(+) repletion
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Direct NAD(+) repletion in neurons either before or after OGD markedly reduced cell death and OGD-induced accumulation of DNA damage (AP sites, single and double strand breaks) in a concentration- and time-dependent manner.
    3 context sentences
    Summary · context
    In vitro ischemic injury was induced in rat primary neuronal cultures by oxygen-glucose deprivation (OGD) for 1 to 2 hours.
    Summary · context
    NAD(+) was replenished by adding NAD(+) directly to the culture medium before or after OGD.
    Summary · context
    Cell viability, oxidative DNA damage, and DNA base-excision repair (BER) activity were measured quantitatively up to 72 hours after OGD with or without NAD(+) repletion.
  4. 04LabIn vitro (cells)Mechanism

    In rat neuronal cultures, NAD(+) repletion reduced oxygen-glucose deprivation-induced double-strand DNA breaks.

    In plain wordsIn cells from rats, NAD(+) repletion reduced double-strand DNA breaks compared with cultures without NAD(+) repletion.

    Outcome
    DecreaseDouble-strand DNA breaks
    Study

    ratn: not reported in source

    Primary neuronal cultures exposed to oxygen-glucose deprivation
    Comparator
    Without NAD(+) repletion
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Direct NAD(+) repletion in neurons either before or after OGD markedly reduced cell death and OGD-induced accumulation of DNA damage (AP sites, single and double strand breaks) in a concentration- and time-dependent manner.
    3 context sentences
    Summary · context
    In vitro ischemic injury was induced in rat primary neuronal cultures by oxygen-glucose deprivation (OGD) for 1 to 2 hours.
    Summary · context
    NAD(+) was replenished by adding NAD(+) directly to the culture medium before or after OGD.
    Summary · context
    Cell viability, oxidative DNA damage, and DNA base-excision repair (BER) activity were measured quantitatively up to 72 hours after OGD with or without NAD(+) repletion.
  5. 05LabIn vitro (cells)Mechanism

    In rat neuronal cultures, NAD(+) repletion restored nuclear DNA repair activity.

    In plain wordsIn cells from rats, NAD(+) repletion restored nuclear DNA repair activity compared with cultures without NAD(+) repletion.

    Outcome
    IncreaseNuclear DNA repair activity
    Study

    ratn: not reported in source

    Primary neuronal cultures exposed to oxygen-glucose deprivation
    Comparator
    Without NAD(+) repletion
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD(+) repletion restored nDNA repair activity by inhibiting serine-specific phosphorylation of the essential BER enzymes AP endonuclease and DNA polymerase-beta.
    3 context sentences
    Summary · context
    In vitro ischemic injury was induced in rat primary neuronal cultures by oxygen-glucose deprivation (OGD) for 1 to 2 hours.
    Summary · context
    NAD(+) was replenished by adding NAD(+) directly to the culture medium before or after OGD.
    Summary · context
    Cell viability, oxidative DNA damage, and DNA base-excision repair (BER) activity were measured quantitatively up to 72 hours after OGD with or without NAD(+) repletion.
  6. 06LabIn vitro (cells)Mechanism

    In rat neuronal cultures, NAD(+) repletion inhibited serine-specific phosphorylation of AP endonuclease.

    In plain wordsIn cells from rats, NAD(+) repletion reduced AP endonuclease phosphorylation compared with cultures without NAD(+) repletion.

    Outcome
    DecreaseAP endonuclease phosphorylation
    Study

    ratn: not reported in source

    Primary neuronal cultures exposed to oxygen-glucose deprivation
    Comparator
    Without NAD(+) repletion
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD(+) repletion restored nDNA repair activity by inhibiting serine-specific phosphorylation of the essential BER enzymes AP endonuclease and DNA polymerase-beta.
    3 context sentences
    Summary · context
    In vitro ischemic injury was induced in rat primary neuronal cultures by oxygen-glucose deprivation (OGD) for 1 to 2 hours.
    Summary · context
    NAD(+) was replenished by adding NAD(+) directly to the culture medium before or after OGD.
    Summary · context
    Cell viability, oxidative DNA damage, and DNA base-excision repair (BER) activity were measured quantitatively up to 72 hours after OGD with or without NAD(+) repletion.
  7. 07LabIn vitro (cells)Mechanism

    In rat neuronal cultures, NAD(+) repletion inhibited serine-specific phosphorylation of DNA polymerase-beta.

    In plain wordsIn cells from rats, NAD(+) repletion reduced DNA polymerase-beta phosphorylation compared with cultures without NAD(+) repletion.

    Outcome
    DecreaseDNA polymerase-beta phosphorylation
    Study

    ratn: not reported in source

    Primary neuronal cultures exposed to oxygen-glucose deprivation
    Comparator
    Without NAD(+) repletion
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD(+) repletion restored nDNA repair activity by inhibiting serine-specific phosphorylation of the essential BER enzymes AP endonuclease and DNA polymerase-beta.
    3 context sentences
    Summary · context
    In vitro ischemic injury was induced in rat primary neuronal cultures by oxygen-glucose deprivation (OGD) for 1 to 2 hours.
    Summary · context
    NAD(+) was replenished by adding NAD(+) directly to the culture medium before or after OGD.
    Summary · context
    Cell viability, oxidative DNA damage, and DNA base-excision repair (BER) activity were measured quantitatively up to 72 hours after OGD with or without NAD(+) repletion.

Studies that did not test the peptide alone1

In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking NAD+ (nicotinamide adenine dinucleotide).

  1. 08LabNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneIn vitro (cells)Mechanism

    In rat neuronal cultures, AP endonuclease knockdown reduced the prosurvival effect of NAD(+) repletion.

    In plain wordsIn cells from rats, AP endonuclease knockdown reduced the survival benefit associated with NAD(+) repletion.

    Outcome
    DecreaseSurvival after AP endonuclease knockdown
    Study

    ratn: not reported in source

    Primary neuronal cultures exposed to oxygen-glucose deprivation
    Outcome group
    Neuroprotection · Nervous system and cognition

    Source sentences

    Summary
    Knocking down AP endonuclease expression significantly reduced the prosurvival effect of NAD(+) repletion.
    3 context sentences
    Summary · context
    Knockdown of BER enzymes was achieved in cultures using AAV-mediated transfection of shRNA.
    Summary · context
    In vitro ischemic injury was induced in rat primary neuronal cultures by oxygen-glucose deprivation (OGD) for 1 to 2 hours.
    Summary · context
    NAD(+) was replenished by adding NAD(+) directly to the culture medium before or after OGD.

    In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).

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

    14 Oct 2026, 05:02 UTC

    Study results updated

  2. Version 1

    14 Oct 2026, 01:46 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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