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Study · In vitro (cells) · 2014

11 results

AMPK inhibition blocks ROS-NFκB signaling and attenuates endotoxemia-induced liver injury.

Guo Y, Zhang Y, Hong K, Luo F, Gu Q, Lu N, Bai A

PloS one24 Jan 2014Cited by 49 (Europe PMC)

PMID24475189 (opens in a new tab)PMCIDPMC3901729 (opens in a new tab)DOI10.1371/journal.pone.0086881 (opens in a new tab)PepBankPUB-24475189
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Summary

BackgroundAMP-activated protein kinase (AMPK) is an important enzyme in regulation of cellular energy homeostasis. We have previously shown that AMPK activation by 5-aminoimidazole-4-carboxamide (AICAR) results in suppression of immune responses, indicating the pivotal role of AMPK in immune regulation. However, the cellular mechanism underpinning AMPK inhibition on immune response remains largely to be elucidated. The study aimed to investigate the effects of AMPK inhibition on reactive oxygen species (ROS)-nuclear factor κB (NFκB) signaling and endotoxemia-induced liver injury.Methodology/principal findingsRAW 264.7 cells were pretreated with AMPK activator or inhibitor, followed by LPS challenge. In addition, LPS was injected intraperitoneally into mice to induce systemic inflammation. The parameters of liver injury and immune responses were determined, and survival of mice was monitored respectively. LPS challenge in RAW 264.7 cells resulted in AMPK activation which was then inhibited by compound C treatment. Both AMPK activation by AICAR or inhibition by compound C diminished LPS-induced ROS generation, inhibited phosphorylation of IKK, IκB, and NFκB p65, and consequently, decreased TNF production of RAW 264.7 cells. AICAR or compound C treatment decreased ALT, AST, and TNF levels in serum, reduced CD68 expression and MPO activity in liver tissue of mice with endotoxemia. Moreover, AICAR or compound C treatment improved survival of endotoxemic mice.ConclusionsAICAR or compound C treatment attenuates LPS-induced ROS-NFκB signaling, immune responses and liver injury. Strategies to activate or inhibit AMPK signaling may provide alternatives to the current clinical approaches to inhibit immune responses of endotoxemia.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study11

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

  1. 01LabIn vitro (cells)Mechanism

    In RAW 264.7 cells, AICAR reduced LPS-induced ROS generation.

    In plain wordsIn cells, AICAR reduced LPS-induced ROS generation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseROS generation
    Study

    n: not reported in source

    LPS-challenged RAW 264.7 cells
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both AMPK activation by AICAR or inhibition by compound C diminished LPS-induced ROS generation, inhibited phosphorylation of IKK, IκB, and NFκB p65, and consequently, decreased TNF production of RAW 264.7 cells.
  2. 02LabIn vitro (cells)Mechanism

    In RAW 264.7 cells, AICAR reduced LPS-induced IKK phosphorylation.

    In plain wordsIn cells, AICAR reduced LPS-induced IKK phosphorylation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseIKK phosphorylation
    Study

    n: not reported in source

    LPS-challenged RAW 264.7 cells
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both AMPK activation by AICAR or inhibition by compound C diminished LPS-induced ROS generation, inhibited phosphorylation of IKK, IκB, and NFκB p65, and consequently, decreased TNF production of RAW 264.7 cells.
  3. 03LabIn vitro (cells)Mechanism

    In RAW 264.7 cells, AICAR reduced LPS-induced IκB phosphorylation.

    In plain wordsIn cells, AICAR reduced LPS-induced IκB phosphorylation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseIκB phosphorylation
    Study

    n: not reported in source

    LPS-challenged RAW 264.7 cells
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both AMPK activation by AICAR or inhibition by compound C diminished LPS-induced ROS generation, inhibited phosphorylation of IKK, IκB, and NFκB p65, and consequently, decreased TNF production of RAW 264.7 cells.
  4. 04LabIn vitro (cells)Mechanism

    In RAW 264.7 cells, AICAR reduced LPS-induced NFκB p65 phosphorylation.

    In plain wordsIn cells, AICAR reduced LPS-induced NFκB p65 phosphorylation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseNFκB p65 phosphorylation
    Study

    n: not reported in source

    LPS-challenged RAW 264.7 cells
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both AMPK activation by AICAR or inhibition by compound C diminished LPS-induced ROS generation, inhibited phosphorylation of IKK, IκB, and NFκB p65, and consequently, decreased TNF production of RAW 264.7 cells.
  5. 05LabIn vitro (cells)Mechanism

    In RAW 264.7 cells, AICAR reduced LPS-induced TNF production.

    In plain wordsIn cells, AICAR reduced LPS-induced TNF production.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseTNF production
    Study

    n: not reported in source

    LPS-challenged RAW 264.7 cells
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both AMPK activation by AICAR or inhibition by compound C diminished LPS-induced ROS generation, inhibited phosphorylation of IKK, IκB, and NFκB p65, and consequently, decreased TNF production of RAW 264.7 cells.

Studies that did not test the peptide alone6

In this study, AICAR (acadesine) 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 AICAR (acadesine).

  1. 06AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In endotoxemic mice, AICAR or compound C decreased serum ALT.

    In plain wordsIn mice with endotoxemia, AICAR or compound C reduced serum ALT.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseSerum ALT
    Study

    mousen: not reported in source

    endotoxemia
    Outcome group
    Liver fat and liver function · Liver

    Source sentences

    Summary
    AICAR or compound C treatment decreased ALT, AST, and TNF levels in serum, reduced CD68 expression and MPO activity in liver tissue of mice with endotoxemia.

    In this study, AICAR (acadesine) 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 AICAR (acadesine).

  2. 07AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In endotoxemic mice, AICAR or compound C decreased serum AST.

    In plain wordsIn mice with endotoxemia, AICAR or compound C reduced serum AST.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseSerum AST
    Study

    mousen: not reported in source

    endotoxemia
    Outcome group
    Liver fat and liver function · Liver

    Source sentences

    Summary
    AICAR or compound C treatment decreased ALT, AST, and TNF levels in serum, reduced CD68 expression and MPO activity in liver tissue of mice with endotoxemia.

    In this study, AICAR (acadesine) 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 AICAR (acadesine).

  3. 08AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In endotoxemic mice, AICAR or compound C decreased serum TNF.

    In plain wordsIn mice with endotoxemia, AICAR or compound C reduced serum TNF.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseSerum TNF
    Study

    mousen: not reported in source

    endotoxemia
    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    AICAR or compound C treatment decreased ALT, AST, and TNF levels in serum, reduced CD68 expression and MPO activity in liver tissue of mice with endotoxemia.

    In this study, AICAR (acadesine) 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 AICAR (acadesine).

  4. 09AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In endotoxemic mice, AICAR or compound C reduced liver CD68 expression.

    In plain wordsIn mice with endotoxemia, AICAR or compound C reduced liver CD68 expression.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseLiver CD68 expression
    Study

    mousen: not reported in source

    endotoxemia
    Outcome group
    Inflammation markers · Liver

    Source sentences

    Summary
    AICAR or compound C treatment decreased ALT, AST, and TNF levels in serum, reduced CD68 expression and MPO activity in liver tissue of mice with endotoxemia.

    In this study, AICAR (acadesine) 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 AICAR (acadesine).

  5. 10AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In endotoxemic mice, AICAR or compound C reduced liver MPO activity.

    In plain wordsIn mice with endotoxemia, AICAR or compound C reduced liver MPO activity.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseLiver MPO activity
    Study

    mousen: not reported in source

    endotoxemia
    Outcome group
    Inflammation markers · Liver

    Source sentences

    Summary
    AICAR or compound C treatment decreased ALT, AST, and TNF levels in serum, reduced CD68 expression and MPO activity in liver tissue of mice with endotoxemia.

    In this study, AICAR (acadesine) 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 AICAR (acadesine).

  6. 11AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Efficacy outcome

    In endotoxemic mice, AICAR or compound C improved survival.

    In plain wordsIn mice with endotoxemia, AICAR or compound C improved survival.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseSurvival
    Study

    mousen: not reported in source

    endotoxemia
    Outcome group
    Mortality · Whole body

    Source sentences

    Summary
    Moreover, AICAR or compound C treatment improved survival of endotoxemic mice.

    In this study, AICAR (acadesine) 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 AICAR (acadesine).

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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