β-Nicotinamide mononucleotide activates NAD+/SIRT1 pathway and attenuates inflammatory and oxidative responses in the hippocampus regions of septic mice.

Li HR, Liu Q, Zhu CL, Sun XY, Sun CY, Yu CM, Li P, Deng XM, Wang JF

Redox biology13 May 2023Cited by 146 (Europe PMC)

PMID37201414PMCIDPMC10206198DOI10.1016/j.redox.2023.102745PepBankPUB-37201414

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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: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study14

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

01AnimalAnimal study (in vivo)Mechanism
In septic mice, NMN reversed the reduction in hippocampal NAD+.
In plain wordsIn septic mice, NMN restored hippocampal NAD+ levels.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseHippocampal NAD+
Study
mousen: not reported in source
cecal ligation and puncture sepsis
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
All these changes induced by sepsis were inverted by NMN.
2 context sentences(design, population, supporting numbers)
Summary · context
As a result, the levels of NAD+, SIRT1 and PGC-1α were significantly reduced in the hippocampus of septic mice, while the acetylation of total lysine, phosphorylation of P38 and P65 were enhanced.
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
Report a problemFND-3720141401
02AnimalAnimal study (in vivo)Mechanism
In septic mice, NMN reversed the reduction in hippocampal SIRT1.
In plain wordsIn septic mice, NMN restored hippocampal SIRT1 levels.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseHippocampal SIRT1
Study
mousen: not reported in source
cecal ligation and puncture sepsis
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
All these changes induced by sepsis were inverted by NMN.
2 context sentences(design, population, supporting numbers)
Summary · context
As a result, the levels of NAD+, SIRT1 and PGC-1α were significantly reduced in the hippocampus of septic mice, while the acetylation of total lysine, phosphorylation of P38 and P65 were enhanced.
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
Report a problemFND-3720141402
03AnimalAnimal study (in vivo)Mechanism
In septic mice, NMN reversed the reduction in hippocampal PGC-1α.
In plain wordsIn septic mice, NMN restored hippocampal PGC-1α levels.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseHippocampal PGC-1α
Study
mousen: not reported in source
cecal ligation and puncture sepsis
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
All these changes induced by sepsis were inverted by NMN.
2 context sentences(design, population, supporting numbers)
Summary · context
As a result, the levels of NAD+, SIRT1 and PGC-1α were significantly reduced in the hippocampus of septic mice, while the acetylation of total lysine, phosphorylation of P38 and P65 were enhanced.
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
Report a problemFND-3720141403
04AnimalAnimal study (in vivo)Mechanism
In septic mice, NMN reversed increased hippocampal total lysine acetylation.
In plain wordsIn septic mice, NMN reduced hippocampal lysine acetylation.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseTotal lysine acetylation
Study
mousen: not reported in source
cecal ligation and puncture sepsis
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
All these changes induced by sepsis were inverted by NMN.
2 context sentences(design, population, supporting numbers)
Summary · context
As a result, the levels of NAD+, SIRT1 and PGC-1α were significantly reduced in the hippocampus of septic mice, while the acetylation of total lysine, phosphorylation of P38 and P65 were enhanced.
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
Report a problemFND-3720141404
05AnimalAnimal study (in vivo)Mechanism
In septic mice, NMN reversed increased hippocampal P38 phosphorylation.
In plain wordsIn septic mice, NMN reduced hippocampal P38 phosphorylation.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseP38 phosphorylation
Study
mousen: not reported in source
cecal ligation and puncture sepsis
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
All these changes induced by sepsis were inverted by NMN.
2 context sentences(design, population, supporting numbers)
Summary · context
As a result, the levels of NAD+, SIRT1 and PGC-1α were significantly reduced in the hippocampus of septic mice, while the acetylation of total lysine, phosphorylation of P38 and P65 were enhanced.
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
Report a problemFND-3720141405
06AnimalAnimal study (in vivo)Mechanism
In septic mice, NMN reversed increased hippocampal P65 phosphorylation.
In plain wordsIn septic mice, NMN reduced hippocampal P65 phosphorylation.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseP65 phosphorylation
Study
mousen: not reported in source
cecal ligation and puncture sepsis
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
All these changes induced by sepsis were inverted by NMN.
2 context sentences(design, population, supporting numbers)
Summary · context
As a result, the levels of NAD+, SIRT1 and PGC-1α were significantly reduced in the hippocampus of septic mice, while the acetylation of total lysine, phosphorylation of P38 and P65 were enhanced.
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
Report a problemFND-3720141406
07AnimalAnimal study (in vivo)Efficacy outcome
In septic mice, NMN improved fear conditioning performance.
In plain wordsIn septic mice, NMN improved fear conditioning test performance.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseFear conditioning performance
Study
mousen: not reported in source
cecal ligation and puncture sepsis
Outcome group
Cognition and memory · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Treating with NMN resulted in improved behavior performance in the fear conditioning tests and Morris water maze.
1 context sentence(design, population, supporting numbers)
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
Report a problemFND-3720141407
08AnimalAnimal study (in vivo)Efficacy outcome
In septic mice, NMN improved Morris water maze performance.
In plain wordsIn septic mice, NMN improved water maze performance.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseMorris water maze performance
Study
mousen: not reported in source
cecal ligation and puncture sepsis
Outcome group
Cognition and memory · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Treating with NMN resulted in improved behavior performance in the fear conditioning tests and Morris water maze.
1 context sentence(design, population, supporting numbers)
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
Report a problemFND-3720141408
09AnimalAnimal study (in vivo)Mechanism
In septic mice, NMN significantly attenuated hippocampal apoptosis.
In plain wordsIn septic mice, NMN reduced hippocampal cell death.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseHippocampal apoptosis
Study
mousen: not reported in source
cecal ligation and puncture sepsis
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Apoptosis, inflammatory and oxidative responses in the hippocampus of septic mice were attenuated significantly after NMN administration.
1 context sentence(design, population, supporting numbers)
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
Report a problemFND-3720141409
10AnimalAnimal study (in vivo)Mechanism
In septic mice, NMN significantly attenuated hippocampal inflammatory responses.
In plain wordsIn septic mice, NMN reduced hippocampal inflammation.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseHippocampal inflammation
Study
mousen: not reported in source
cecal ligation and puncture sepsis
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Apoptosis, inflammatory and oxidative responses in the hippocampus of septic mice were attenuated significantly after NMN administration.
1 context sentence(design, population, supporting numbers)
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
Report a problemFND-3720141410
11AnimalAnimal study (in vivo)Mechanism
In septic mice, NMN significantly attenuated hippocampal oxidative responses.
In plain wordsIn septic mice, NMN reduced hippocampal oxidative responses.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseHippocampal oxidative responses
Study
mousen: not reported in source
cecal ligation and puncture sepsis
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Apoptosis, inflammatory and oxidative responses in the hippocampus of septic mice were attenuated significantly after NMN administration.
1 context sentence(design, population, supporting numbers)
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
Report a problemFND-3720141411
12LabIn vitro (cells)Mechanism
In LPS-treated BV-2 cells, NMN attenuated cell activation.
In plain wordsIn cells exposed to LPS, NMN reduced BV-2 cell activation.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseBV-2 activation
Study
n: not reported in source
LPS-treated BV-2 cells
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
Similarly, LPS-induced activation of BV-2 cells were attenuated by NMN, EX-527 or SIRT1 knockdown could reverse such effect of NMN in vitro.
1 context sentence(design, population, supporting numbers)
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
Report a problemFND-3720141413

Studies that did not test the peptide alone2

In this study, NMN (nicotinamide mononucleotide) 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 NMN (nicotinamide mononucleotide).

13AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism
In septic mice, EX-527 reversed NMN protection against memory dysfunction and inflammatory and oxidative injuries.
In plain wordsIn septic mice, a SIRT1 inhibitor reversed NMN protection against memory problems and inflammatory and oxidative injuries.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
Not applicableSIRT1 dependence
Study
mousen: not reported in source
cecal ligation and puncture sepsis
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
These protective effect of NMN against memory dysfunction, inflammatory and oxidative injuries were reversed by the SIRT1 inhibitor, EX-527.
1 context sentence(design, population, supporting numbers)
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
In this study, NMN (nicotinamide mononucleotide) 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 NMN (nicotinamide mononucleotide).
Report a problemFND-3720141412
14LabNot a test of NMN (nicotinamide mononucleotide) aloneIn vitro (cells)Mechanism
In BV-2 cells, EX-527 or SIRT1 knockdown reversed NMN effects on LPS-induced activation.
In plain wordsIn cells, SIRT1 inhibition or gene suppression reversed NMN effects on LPS-induced activation.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
Not applicableSIRT1 dependence of BV-2 activation
Study
n: not reported in source
LPS-treated BV-2 cells
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Similarly, LPS-induced activation of BV-2 cells were attenuated by NMN, EX-527 or SIRT1 knockdown could reverse such effect of NMN in vitro.
1 context sentence(design, population, supporting numbers)
Summary · context
The SAE model was established by cecal ligation and puncture (CLP) in vivo, and neuroinflammation model was established with LPS-treated BV-2 cells in vitro.
In this study, NMN (nicotinamide mononucleotide) 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 NMN (nicotinamide mononucleotide).
Report a problemFND-3720141414

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
21 Oct 2026, 15:58 UTC
Study results updated
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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