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Study · Ex vivo tissue · mouse · 2011

2 results

Suppression of leukocyte infiltration and cartilage degradation by selective inhibition of pre-B cell colony-enhancing factor/visfatin/nicotinamide phosphoribosyltransferase: Apo866-mediated therapy in human fibroblasts and murine collagen-induced arthritis.

Evans L, Williams AS, Hayes AJ, Jones SA, Nowell M

Arthritis and rheumatism1 Jul 2011Cited by 45 (Europe PMC)

PMID21400478 (opens in a new tab)DOI10.1002/art.30338 (opens in a new tab)PepBankPUB-21400478
Publisher pagePubMedAsk about this study
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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: Publisher copyright. Results still quote short attributed sentences.

Results from this study2

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

  1. 01LabEx vivo tissueMechanism

    In synovial explants from arthritic mice, NMN reversed APO866-induced inhibition of CCL2 production.

    In plain wordsIn lab tests of arthritic mouse tissue, NMN reversed the reduction in CCL2 production caused by APO866.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseCCL2 production
    Study

    mousen: not reported in source

    Synovial explants from arthritic mice
    Comparator
    APO866-treated synovial explants
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, APO866 reduced the activity of MMP-3, CCL2, and RANKL in vivo, and inhibited production of CCL2 and RANKL in synovial explants from arthritic mice, a result that was reversed with nicotinamide mononucleotide.
  2. 02LabEx vivo tissueMechanism

    In synovial explants from arthritic mice, NMN reversed APO866-induced inhibition of RANKL production.

    In plain wordsIn lab tests of arthritic mouse tissue, NMN reversed the reduction in RANKL production caused by APO866.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseRANKL production
    Study

    mousen: not reported in source

    Synovial explants from arthritic mice
    Comparator
    APO866-treated synovial explants
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, APO866 reduced the activity of MMP-3, CCL2, and RANKL in vivo, and inhibited production of CCL2 and RANKL in synovial explants from arthritic mice, a result that was reversed with nicotinamide mononucleotide.

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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