Exogenous NAD(+) supplementation protects H9c2 cardiac myoblasts against hypoxia/reoxygenation injury via Sirt1-p53 pathway.

Liu L, Wang P, Liu X, He D, Liang C, Yu Y

Fundamental & clinical pharmacology6 Feb 2013Cited by 42 (Europe PMC)

PMID23384296DOI10.1111/fcp.12016PepBankPUB-23384296

Publisher page PubMedAsk about this study

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 study7

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

01LabIn vitro (cells)Mechanism
In HR-stressed H9c2 cells, exogenous NAD increased intracellular NAD in time- and concentration-dependent manners.
In plain wordsIn cells, NAD increased intracellular NAD in time- and concentration-dependent manners.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
IncreaseIntracellular NAD level
Study
n: not reported in source
HR-stressed H9c2 cardiac myoblasts
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
Exogenous NAD(+) supplementation elevated intracellular NAD(+) level and reduced HR-induced cell death in both time- and concentration-dependent manners.
1 context sentence(design, population, supporting numbers)
Summary · context
The objective of this study was to investigate the role of exogenous NAD(+) supplementation in hypoxia/reoxygenation (HR)-stressed H9c2 cardiac myoblasts.
Report a problemFND-2338429601
02LabIn vitro (cells)Efficacy outcome
In HR-stressed H9c2 cells, NAD reduced cell death in time- and concentration-dependent manners.
In plain wordsIn cells, NAD reduced death after hypoxia and reoxygenation in time- and concentration-dependent manners.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseCell death
Study
n: not reported in source
HR-stressed H9c2 cardiac myoblasts
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
Exogenous NAD(+) supplementation elevated intracellular NAD(+) level and reduced HR-induced cell death in both time- and concentration-dependent manners.
1 context sentence(design, population, supporting numbers)
Summary · context
The objective of this study was to investigate the role of exogenous NAD(+) supplementation in hypoxia/reoxygenation (HR)-stressed H9c2 cardiac myoblasts.
Report a problemFND-2338429602
03LabIn vitro (cells)Efficacy outcome
In HR-stressed H9c2 cells, NAD gave greatest protection at 500 to 1000 μm when added immediately after reoxygenation began.
In plain wordsIn cells, NAD gave greatest protection at 500 to 1000 μm when added immediately after reoxygenation began.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
Not applicableOptimal cytoprotection conditions
Study
n: not reported in source
HR-stressed H9c2 cardiac myoblasts
Outcome group
Heart function · Cardiovascular
Studied dose
500 to 1000 μmAs given in this study.
Source sentences
Summary
It appeared that NAD(+) supplementation exerted the greatest protection when extracellular concentration ranged from 500 to 1000 μm and when NAD(+) was added immediately after reoxygenation began.
1 context sentence(design, population, supporting numbers)
Summary · context
The objective of this study was to investigate the role of exogenous NAD(+) supplementation in hypoxia/reoxygenation (HR)-stressed H9c2 cardiac myoblasts.
Report a problemFND-2338429603
04LabIn vitro (cells)Mechanism
In HR-stressed H9c2 cells, NAD replenishment restored Sirt1 activity.
In plain wordsIn cells, NAD restored Sirt1 activity after hypoxia and reoxygenation.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
IncreaseSirt1 activity
Study
n: not reported in source
HR-stressed H9c2 cardiac myoblasts
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
NAD(+) replenishment restored Sirt1 activity, reduced the acetylation level of p53 (Lys373 & 382), and attenuated cell apoptosis in HR-stressed H9c2 cells, whereas inhibition of Sirt1 activity alleviated the effects of NAD(+) replenishment.
1 context sentence(design, population, supporting numbers)
Summary · context
The objective of this study was to investigate the role of exogenous NAD(+) supplementation in hypoxia/reoxygenation (HR)-stressed H9c2 cardiac myoblasts.
Report a problemFND-2338429604
05LabIn vitro (cells)Mechanism
In HR-stressed H9c2 cells, NAD reduced p53 acetylation at Lys373 and 382.
In plain wordsIn cells, NAD reduced p53 acetylation after hypoxia and reoxygenation.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
Decreasep53 acetylation
Study
n: not reported in source
HR-stressed H9c2 cardiac myoblasts
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
NAD(+) replenishment restored Sirt1 activity, reduced the acetylation level of p53 (Lys373 & 382), and attenuated cell apoptosis in HR-stressed H9c2 cells, whereas inhibition of Sirt1 activity alleviated the effects of NAD(+) replenishment.
1 context sentence(design, population, supporting numbers)
Summary · context
The objective of this study was to investigate the role of exogenous NAD(+) supplementation in hypoxia/reoxygenation (HR)-stressed H9c2 cardiac myoblasts.
Report a problemFND-2338429605
06LabIn vitro (cells)Efficacy outcome
In HR-stressed H9c2 cells, NAD replenishment attenuated apoptosis.
In plain wordsIn cells, NAD reduced apoptosis after hypoxia and reoxygenation.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseCell apoptosis
Study
n: not reported in source
HR-stressed H9c2 cardiac myoblasts
Outcome group
Heart function · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
NAD(+) replenishment restored Sirt1 activity, reduced the acetylation level of p53 (Lys373 & 382), and attenuated cell apoptosis in HR-stressed H9c2 cells, whereas inhibition of Sirt1 activity alleviated the effects of NAD(+) replenishment.
1 context sentence(design, population, supporting numbers)
Summary · context
The objective of this study was to investigate the role of exogenous NAD(+) supplementation in hypoxia/reoxygenation (HR)-stressed H9c2 cardiac myoblasts.
Report a problemFND-2338429606

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).

07LabNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneIn vitro (cells)Mechanism
In HR-stressed H9c2 cells, Sirt1 inhibition alleviated the effects of NAD replenishment.
In plain wordsIn cells, Sirt1 inhibition reduced the effects of NAD replenishment.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseSirt1 inhibition of NAD protection
Study
n: not reported in source
HR-stressed H9c2 cardiac myoblasts
Outcome group
Heart function · Cardiovascular
Source sentences
Summary
NAD(+) replenishment restored Sirt1 activity, reduced the acetylation level of p53 (Lys373 & 382), and attenuated cell apoptosis in HR-stressed H9c2 cells, whereas inhibition of Sirt1 activity alleviated the effects of NAD(+) replenishment.
1 context sentence(design, population, supporting numbers)
Summary · context
The objective of this study was to investigate the role of exogenous NAD(+) supplementation in hypoxia/reoxygenation (HR)-stressed H9c2 cardiac myoblasts.
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).
Report a problemFND-2338429607

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
14 Oct 2026, 05:02 UTC
Study results updated
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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