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Study · Animal study (in vivo) · mouse · 2025

12 results

Nicotinamide mononucleotide ameliorates hypertriglyceridemia pancreatitis via NAD+/SIRT1-mediated TXNIP suppression and NOTCH pathway for accelerated repair-associated processes.

Duan H, Zhang R, Asikaer A, Pan L, Wang S, Huang K, Lou D, Wang Y, Lin Z, Shen Y

International immunopharmacology10 Apr 2025Cited by 5 (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 study12

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice, repeated NMN ameliorated P407- and caerulein-induced pancreatic injury.

    In plain wordsIn mice, repeated NMN reduced pancreatic injury caused by P407 and caerulein.

    Outcome
    DecreasePancreatic injury
    Study

    mousen: not reported in source

    P407- and caerulein-induced pancreatitis
    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Repeated administration of NMN significantly ameliorated P407 and caerulein (CER)-induced pancreatic injury and dysfunction in mice.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice, repeated NMN ameliorated P407- and caerulein-induced pancreatic dysfunction.

    In plain wordsIn mice, repeated NMN reduced pancreatic dysfunction caused by P407 and caerulein.

    Outcome
    DecreasePancreatic dysfunction
    Study

    mousen: not reported in source

    P407- and caerulein-induced pancreatitis
    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Repeated administration of NMN significantly ameliorated P407 and caerulein (CER)-induced pancreatic injury and dysfunction in mice.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mice with pancreatitis, NMN showed potential to reduce inflammatory responses.

    In plain wordsIn mice with pancreatitis, NMN showed potential to reduce inflammation.

    Outcome
    DecreaseInflammatory responses
    Study

    mousen: not reported in source

    P407- and caerulein-induced pancreatitis
    Outcome group
    Inflammation markers · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Consistently, NMN exhibited the potential to reduce inflammatory responses, lower serum lipid levels, and mitigate the accumulation of reactive oxygen species (ROS).
    1 context sentence
    Summary · context
    Repeated administration of NMN significantly ameliorated P407 and caerulein (CER)-induced pancreatic injury and dysfunction in mice.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In mice with pancreatitis, NMN showed potential to lower serum lipid levels.

    In plain wordsIn mice with pancreatitis, NMN showed potential to lower blood fat levels.

    Outcome
    DecreaseSerum lipids
    Study

    mousen: not reported in source

    P407- and caerulein-induced pancreatitis
    Outcome group
    Lipids · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Consistently, NMN exhibited the potential to reduce inflammatory responses, lower serum lipid levels, and mitigate the accumulation of reactive oxygen species (ROS).
    1 context sentence
    Summary · context
    Repeated administration of NMN significantly ameliorated P407 and caerulein (CER)-induced pancreatic injury and dysfunction in mice.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mice with pancreatitis, NMN showed potential to mitigate ROS accumulation.

    In plain wordsIn mice with pancreatitis, NMN showed potential to reduce reactive oxygen accumulation.

    Outcome
    DecreaseROS accumulation
    Study

    mousen: not reported in source

    P407- and caerulein-induced pancreatitis
    Outcome group
    Mitochondrial function · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Consistently, NMN exhibited the potential to reduce inflammatory responses, lower serum lipid levels, and mitigate the accumulation of reactive oxygen species (ROS).
    1 context sentence
    Summary · context
    Repeated administration of NMN significantly ameliorated P407 and caerulein (CER)-induced pancreatic injury and dysfunction in mice.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In mice during pancreatic repair, sustained NMN inhibited the NOTCH pathway.

    In plain wordsIn mice during pancreatic repair, sustained NMN inhibited the NOTCH pathway.

    Outcome
    DecreaseNOTCH pathway
    Study

    mousen: not reported in source

    Pancreatic repair phase
    Outcome group
    Receptor activity and mechanism · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    More importantly, sustained NMN treatment inhibited the NOTCH pathway and promoted M2-type macrophage dominance during the pancreatic repair phase, influencing early or late macrophage polarization, which significantly enhanced inflammation resolution.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In mice during pancreatic repair, sustained NMN promoted M2-type macrophage dominance.

    In plain wordsIn mice during pancreatic repair, sustained NMN increased dominance of M2-type macrophages.

    Outcome
    IncreaseM2-type macrophage dominance
    Study

    mousen: not reported in source

    Pancreatic repair phase
    Outcome group
    Immune response · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    More importantly, sustained NMN treatment inhibited the NOTCH pathway and promoted M2-type macrophage dominance during the pancreatic repair phase, influencing early or late macrophage polarization, which significantly enhanced inflammation resolution.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In mice during pancreatic repair, sustained NMN significantly enhanced inflammation resolution.

    In plain wordsIn mice during pancreatic repair, sustained NMN improved resolution of inflammation.

    Outcome
    IncreaseInflammation resolution
    Study

    mousen: not reported in source

    Pancreatic repair phase
    Outcome group
    Inflammation markers · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    More importantly, sustained NMN treatment inhibited the NOTCH pathway and promoted M2-type macrophage dominance during the pancreatic repair phase, influencing early or late macrophage polarization, which significantly enhanced inflammation resolution.
  9. 09LabIn vitro (cells)Mechanism

    In pancreatic acinar cells, NMN rescued oleic- and palmitic-acid-induced mitochondrial dysfunction.

    In plain wordsIn cells, NMN reduced mitochondrial dysfunction caused by oleic and palmitic acids.

    Outcome
    DecreaseMitochondrial dysfunction
    Study

    n: not reported in source

    OA- and PA-treated pancreatic acinar cells
    Outcome group
    Mitochondrial function · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro studies revealed that NMN rescued oleic acid (OA)- and palmitic acid (PA)-induced mitochondrial dysfunction and cellular injury in pancreatic acinar cells by suppressing thioredoxin-interacting protein (TXNIP) through NAD+/sirtuin 1 (SIRT1) signaling.
  10. 10LabIn vitro (cells)Mechanism

    In pancreatic acinar cells, NMN rescued oleic- and palmitic-acid-induced cellular injury.

    In plain wordsIn cells, NMN reduced injury caused by oleic and palmitic acids.

    Outcome
    DecreaseCellular injury
    Study

    n: not reported in source

    OA- and PA-treated pancreatic acinar cells
    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro studies revealed that NMN rescued oleic acid (OA)- and palmitic acid (PA)-induced mitochondrial dysfunction and cellular injury in pancreatic acinar cells by suppressing thioredoxin-interacting protein (TXNIP) through NAD+/sirtuin 1 (SIRT1) signaling.
  11. 11LabIn vitro (cells)Mechanism

    In pancreatic acinar cells, NMN suppressed TXNIP through NAD+/SIRT1 signaling.

    In plain wordsIn cells, NMN suppressed TXNIP through NAD+/SIRT1 signaling.

    Outcome
    DecreaseTXNIP suppression
    Study

    n: not reported in source

    OA- and PA-treated pancreatic acinar cells
    Outcome group
    Receptor activity and mechanism · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro studies revealed that NMN rescued oleic acid (OA)- and palmitic acid (PA)-induced mitochondrial dysfunction and cellular injury in pancreatic acinar cells by suppressing thioredoxin-interacting protein (TXNIP) through NAD+/sirtuin 1 (SIRT1) signaling.
  12. 12LabIn vitro (cells)Mechanism

    In BMDM, RAW 264.7 and THP-1 cell models, NMN influenced macrophage phenotype through the NOTCH pathway.

    In plain wordsIn cells, NMN changed macrophage phenotype through the NOTCH pathway.

    Outcome
    MixedMacrophage phenotype
    Study

    mouse and humann: not reported in source

    BMDM, RAW 264.7 and THP-1 cells
    Outcome group
    Immune response · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    As expected, in vitro models using mouse bone marrow-derived macrophage (BMDM), RAW 264.7, and THP-1 cells confirmed that NMN influences macrophage phenotype through the NOTCH pathway.

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

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. 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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