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Study · In vitro (cells) · 2021

6 results

Nicotinamide Mononucleotide Alleviates LPS-Induced Inflammation and Oxidative Stress via Decreasing COX-2 Expression in Macrophages.

Liu J, Zong Z, Zhang W, Chen Y, Wang X, Shen J, Yang C, Liu X, Deng H

Frontiers in molecular biosciences6 Jul 2021Cited by 46 (Europe PMC)

PMID34295923 (opens in a new tab)PMCIDPMC8290259 (opens in a new tab)DOI10.3389/fmolb.2021.702107 (opens in a new tab)PepBankPUB-34295923
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Summary

Macrophage activation is an important process in controlling infection, but persistent macrophage activation leads to chronic inflammation and diseases, such as tumor progression, insulin resistance and atherosclerosis. Characterizing metabolic signatures of macrophage activation is important for developing new approaches for macrophage inactivation. Herein, we performed metabolomic analysis on lipopolysaccharide (LPS)-activated macrophages and identified the associated changes in metabolites. Notably, the cellular Nicotinamide adenine dinucleotide+ levels were decreased while NADPH was increased, proposing that NAD+ restoration can inhibit macrophage activation. Indeed, supplementation of nicotinamide mononucleotide (NMN) increased cellular NAD+ levels and decreased cytokine productions in LPS-activated cells. Quantitative proteomics identified that nicotinamide mononucleotide downregulated the expressions of LPS-responsive proteins, in which cyclooxygenase-2 (COX-2) expression was significantly decreased in NMN-treated cells. Consequently, the cellular levels of prostaglandin E2 (PGE2) was also decreased, indicating that NMN inactivated macrophages via COX-2-PGE2 pathway, which was validated in activated THP-1 cells and mouse peritoneal macrophages. In conclusion, the present study identified the metabolic characteristics of activated macrophages and revealed that NMN replenishment is an efficient approach for controlling macrophage activation.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

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

  1. 01LabIn vitro (cells)Mechanism

    In LPS-activated macrophages, NMN increased cellular NAD+ levels.

    In plain wordsIn cells, NMN increased NAD+ levels compared with LPS activation alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseCellular NAD+
    Study

    n: not reported in source

    LPS-activated macrophages
    Comparator
    LPS activation without NMN
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Indeed, supplementation of nicotinamide mononucleotide (NMN) increased cellular NAD+ levels and decreased cytokine productions in LPS-activated cells.
  2. 02LabIn vitro (cells)Mechanism

    In LPS-activated macrophages, NMN decreased cytokine production.

    In plain wordsIn cells, NMN decreased cytokine production compared with LPS activation alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseCytokine production
    Study

    n: not reported in source

    LPS-activated macrophages
    Comparator
    LPS activation without NMN
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Indeed, supplementation of nicotinamide mononucleotide (NMN) increased cellular NAD+ levels and decreased cytokine productions in LPS-activated cells.
  3. 03LabIn vitro (cells)Mechanism

    In LPS-activated macrophages, NMN reduced expression of LPS-responsive proteins.

    In plain wordsIn cells, NMN reduced LPS-responsive protein expression compared with LPS activation alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseLPS-responsive protein expression
    Study

    n: not reported in source

    LPS-activated macrophages
    Comparator
    LPS activation without NMN
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Quantitative proteomics identified that nicotinamide mononucleotide downregulated the expressions of LPS-responsive proteins, in which cyclooxygenase-2 (COX-2) expression was significantly decreased in NMN-treated cells.
  4. 04LabIn vitro (cells)Mechanism

    In LPS-activated macrophages, NMN significantly reduced COX-2 expression.

    In plain wordsIn cells, NMN reduced COX-2 expression compared with LPS activation alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseCOX-2 expression
    Study

    n: not reported in source

    LPS-activated macrophages
    Comparator
    LPS activation without NMN
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Quantitative proteomics identified that nicotinamide mononucleotide downregulated the expressions of LPS-responsive proteins, in which cyclooxygenase-2 (COX-2) expression was significantly decreased in NMN-treated cells.
  5. 05LabIn vitro (cells)Mechanism

    In activated macrophages, NMN decreased cellular prostaglandin E2 levels.

    In plain wordsIn cells, NMN reduced prostaglandin E2 levels compared with activation without NMN.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseProstaglandin E2 levels
    Study

    n: not reported in source

    LPS-activated macrophages
    Comparator
    LPS activation without NMN
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Consequently, the cellular levels of prostaglandin E2 (PGE2) was also decreased, indicating that NMN inactivated macrophages via COX-2-PGE2 pathway, which was validated in activated THP-1 cells and mouse peritoneal macrophages.
  6. 06LabIn vitro (cells)Mechanism

    In activated THP-1 cells and mouse peritoneal macrophages, NMN inactivated macrophages through the COX-2-PGE2 pathway.

    In plain wordsIn cells, NMN reduced macrophage activation through the COX-2-PGE2 pathway compared with activation without NMN.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMacrophage inactivation through COX-2-PGE2
    Study

    n: not reported in source

    Activated THP-1 cells and mouse peritoneal macrophages
    Comparator
    LPS activation without NMN
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Consequently, the cellular levels of prostaglandin E2 (PGE2) was also decreased, indicating that NMN inactivated macrophages via COX-2-PGE2 pathway, which was validated in activated THP-1 cells and mouse peritoneal macrophages.

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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