Study · Animal study (in vivo) · mouse · 2022
7 resultsLuo C, Ding W, Yang C, Zhang W, Liu X, Deng H
Journal of proteome research14 Jun 2022Cited by 30 (Europe PMC)
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Text rights: Publisher copyright. Results still quote short attributed sentences.
6 results from studies that gave the peptide. No result from this study comes from people.
In aged mice, NMN decreased liver oxidative stress.
In plain wordsIn mice, NMN reduced liver oxidative stress.
mousen: not reported in source
aged mouse liverSource sentences
Importantly, nicotinamide mononucleotide (NMN) administration decreased the oxidative stress and the nuclear Nrf2 and Nrf2 downstream gene levels.
In aged mice, NMN decreased nuclear Nrf2 levels.
In plain wordsIn mice, NMN reduced nuclear Nrf2 levels.
mousen: not reported in source
aged mouse liverSource sentences
Importantly, nicotinamide mononucleotide (NMN) administration decreased the oxidative stress and the nuclear Nrf2 and Nrf2 downstream gene levels.
In aged mice, NMN decreased Nrf2 downstream gene levels.
In plain wordsIn mice, NMN reduced Nrf2 downstream gene levels.
mousen: not reported in source
aged mouse liverSource sentences
Importantly, nicotinamide mononucleotide (NMN) administration decreased the oxidative stress and the nuclear Nrf2 and Nrf2 downstream gene levels.
In aged mice, NMN improved resistance to acetaminophen-induced liver injury.
In plain wordsIn mice, NMN improved resistance to acetaminophen-induced liver injury.
mousen: not reported in source
aged mouse liverSource sentences
Indeed, aged mice treated with NMN improved stress resistance against acetaminophen (APAP)-induced liver injury, indicating that NMN restored Nrf2-mediated adaptive homeostasis.
In aged mice, NMN increased Sirt3 activity.
In plain wordsIn mice, NMN increased Sirt3 activity.
mousen: not reported in source
aged mouse liverSource sentences
Further studies found that NMN increased Sirt3 activities to deacetylate age-associated acetylation at K68 and K122 in Sod2, while its effects on nuclear Nrf2 levels were diminished in Sirt3-deficient mice, suggesting that NMN-enhanced adaptive homeostasis was Sirt3-dependent.
In aged mice, NMN increased Sirt3-mediated deacetylation at Sod2 K68 and K122.
In plain wordsIn mice, NMN increased removal of acetyl groups at Sod2 K68 and K122.
mousen: not reported in source
aged mouse liverSource sentences
Further studies found that NMN increased Sirt3 activities to deacetylate age-associated acetylation at K68 and K122 in Sod2, while its effects on nuclear Nrf2 levels were diminished in Sirt3-deficient mice, suggesting that NMN-enhanced adaptive homeostasis was Sirt3-dependent.
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).
In Sirt3-deficient mice, NMN effects on nuclear Nrf2 levels diminished.
In plain wordsIn mice with Sirt3 deficiency, NMN had a smaller effect on nuclear Nrf2 levels.
mousen: not reported in source
aged mouse liverSource sentences
Further studies found that NMN increased Sirt3 activities to deacetylate age-associated acetylation at K68 and K122 in Sod2, while its effects on nuclear Nrf2 levels were diminished in Sirt3-deficient mice, suggesting that NMN-enhanced adaptive homeostasis was Sirt3-dependent.
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).
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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
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