β-Nicotinamide Mononucleotide Alleviates Sepsis-associated Acute Kidney Injury by Activating NAD+/SIRT3 Signaling.

Sun C, Xiong H, Guo T

Cell biochemistry and biophysics23 Nov 2024Cited by 5 (Europe PMC)

PMID39580586DOI10.1007/s12013-024-01619-9PepBankPUB-39580586

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

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

01AnimalAnimal study (in vivo)Mechanism
In mice with septic kidney injury, β-NMN increased renal NAD+ levels.
In plain wordsIn mice with septic kidney injury, β-NMN increased kidney NAD+ levels.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseRenal NAD+
Study
mousen: not reported in source
CLP-induced sepsis-associated AKI
Outcome group
Receptor activity and mechanism · Kidney and urinary
Studied dose
Dose not stated
Source sentences
Summary
β-NMN treatment increased NAD+ level and alleviated the inflammation and apoptosis in renal tissues.
1 context sentence(design, population, supporting numbers)
Summary · context
A cecal ligation and perforation (CLP)-induced sepsis-associated AKI mice model and a lipopolysaccharide (LPS)-triggered HK-2 cell model were established.
Report a problemFND-3958058601
02AnimalAnimal study (in vivo)Mechanism
In mice with septic kidney injury, β-NMN alleviated renal inflammation.
In plain wordsIn mice with septic kidney injury, β-NMN reduced kidney inflammation.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseRenal inflammation
Study
mousen: not reported in source
CLP-induced sepsis-associated AKI
Outcome group
Inflammation markers · Kidney and urinary
Studied dose
Dose not stated
Source sentences
Summary
β-NMN treatment increased NAD+ level and alleviated the inflammation and apoptosis in renal tissues.
1 context sentence(design, population, supporting numbers)
Summary · context
A cecal ligation and perforation (CLP)-induced sepsis-associated AKI mice model and a lipopolysaccharide (LPS)-triggered HK-2 cell model were established.
Report a problemFND-3958058602
03AnimalAnimal study (in vivo)Mechanism
In mice with septic kidney injury, β-NMN alleviated renal apoptosis.
In plain wordsIn mice with septic kidney injury, β-NMN reduced programmed death of kidney cells.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseRenal apoptosis
Study
mousen: not reported in source
CLP-induced sepsis-associated AKI
Outcome group
Kidney function · Kidney and urinary
Studied dose
Dose not stated
Source sentences
Summary
β-NMN treatment increased NAD+ level and alleviated the inflammation and apoptosis in renal tissues.
1 context sentence(design, population, supporting numbers)
Summary · context
A cecal ligation and perforation (CLP)-induced sepsis-associated AKI mice model and a lipopolysaccharide (LPS)-triggered HK-2 cell model were established.
Report a problemFND-3958058603
04AnimalAnimal study (in vivo)Mechanism
In mice with septic kidney injury, β-NMN increased SIRT3 expression.
In plain wordsIn mice with septic kidney injury, β-NMN increased SIRT3 expression.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseRenal SIRT3 expression
Study
mousen: not reported in source
CLP-induced sepsis-associated AKI
Outcome group
Receptor activity and mechanism · Kidney and urinary
Studied dose
Dose not stated
Source sentences
Summary
It could be observed that SIRT3 expression was notably downregulated in vivo and in vitro, which was upregulated by β-NMN supplementation.
1 context sentence(design, population, supporting numbers)
Summary · context
A cecal ligation and perforation (CLP)-induced sepsis-associated AKI mice model and a lipopolysaccharide (LPS)-triggered HK-2 cell model were established.
Report a problemFND-3958058604
05LabIn vitro (cells)Mechanism
In LPS-treated HK-2 cells, β-NMN increased SIRT3 expression.
In plain wordsIn cells treated with LPS, β-NMN increased SIRT3 expression.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
IncreaseSIRT3 expression
Study
humann: not reported in source
LPS-treated HK-2 cells
Outcome group
Receptor activity and mechanism · Kidney and urinary
Studied dose
Dose not stated
Source sentences
Summary
It could be observed that SIRT3 expression was notably downregulated in vivo and in vitro, which was upregulated by β-NMN supplementation.
1 context sentence(design, population, supporting numbers)
Summary · context
A cecal ligation and perforation (CLP)-induced sepsis-associated AKI mice model and a lipopolysaccharide (LPS)-triggered HK-2 cell model were established.
Report a problemFND-3958058605

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).

06LabNot a test of NMN (nicotinamide mononucleotide) aloneIn vitro (cells)Mechanism
In LPS-treated HK-2 cells, SIRT3 interference weakened β-NMN protection against inflammation.
In plain wordsIn cells treated with LPS, SIRT3 interference weakened β-NMN protection against inflammation.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseSIRT3-dependent inflammation protection
Study
humann: not reported in source
LPS-treated HK-2 cells with SIRT3 silencing
Outcome group
Inflammation markers · Kidney and urinary
Source sentences
Summary
Further, interfering with SIRT3 expression mitigated the protective effects of β-NMN on the inflammation and apoptosis of HK-2 cells under LPS conditions.
1 context sentence(design, population, supporting numbers)
Summary · context
A cecal ligation and perforation (CLP)-induced sepsis-associated AKI mice model and a lipopolysaccharide (LPS)-triggered HK-2 cell model were established.
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-3958058606
07LabNot a test of NMN (nicotinamide mononucleotide) aloneIn vitro (cells)Mechanism
In LPS-treated HK-2 cells, SIRT3 interference weakened β-NMN protection against apoptosis.
In plain wordsIn cells treated with LPS, SIRT3 interference weakened β-NMN protection against programmed cell death.
Peptide
NMN (nicotinamide mononucleotide)
Outcome
DecreaseSIRT3-dependent apoptosis protection
Study
humann: not reported in source
LPS-treated HK-2 cells with SIRT3 silencing
Outcome group
Receptor activity and mechanism · Kidney and urinary
Source sentences
Summary
Further, interfering with SIRT3 expression mitigated the protective effects of β-NMN on the inflammation and apoptosis of HK-2 cells under LPS conditions.
1 context sentence(design, population, supporting numbers)
Summary · context
A cecal ligation and perforation (CLP)-induced sepsis-associated AKI mice model and a lipopolysaccharide (LPS)-triggered HK-2 cell model were established.
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-3958058607

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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