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Study · Animal study (in vivo) · mouse · 2017

10 results

AMPK activation ameliorates D-GalN/LPS-induced acute liver failure by upregulating Foxo3A to induce autophagy.

Liu YM, Lv J, Zeng QL, Shen S, Xing JY, Zhang YY, Zhang ZH, Yu ZJ

Experimental cell research6 Jul 2017Cited by 23 (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 study10

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice with induced acute liver failure, AICAR-mediated AMPK activation ameliorated liver failure.

    In plain wordsIn mice, AMPK activation with AICAR reduced induced liver failure.

    Outcome
    DecreaseAcute liver failure
    Study

    mousen: not reported in source

    D-GalN/LPS-induced acute liver failure
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activation ameliorated ALF by inhibiting inflammation (downregulated TNF-α, IL-1β and IL-6 expression), activating autophagy (increased Atg-5, Beclin-1 and Atg-7 expression) and upregulating Foxo3A expression.
    1 context sentence
    Summary · context
    AMPK activation and inhibition of autophagy were induced by AICAR and 3-MA, respectively.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mice with acute liver failure, AICAR-mediated AMPK activation decreased TNF-α expression.

    In plain wordsIn mice, AMPK activation with AICAR reduced TNF-α expression during liver failure.

    Outcome
    DecreaseTNF-alpha expression
    Study

    mousen: not reported in source

    D-GalN/LPS-induced acute liver failure
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activation ameliorated ALF by inhibiting inflammation (downregulated TNF-α, IL-1β and IL-6 expression), activating autophagy (increased Atg-5, Beclin-1 and Atg-7 expression) and upregulating Foxo3A expression.
    1 context sentence
    Summary · context
    AMPK activation and inhibition of autophagy were induced by AICAR and 3-MA, respectively.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mice with acute liver failure, AICAR-mediated AMPK activation decreased IL-1β expression.

    In plain wordsIn mice, AMPK activation with AICAR reduced IL-1β expression during liver failure.

    Outcome
    DecreaseIL-1beta expression
    Study

    mousen: not reported in source

    D-GalN/LPS-induced acute liver failure
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activation ameliorated ALF by inhibiting inflammation (downregulated TNF-α, IL-1β and IL-6 expression), activating autophagy (increased Atg-5, Beclin-1 and Atg-7 expression) and upregulating Foxo3A expression.
    1 context sentence
    Summary · context
    AMPK activation and inhibition of autophagy were induced by AICAR and 3-MA, respectively.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In mice with acute liver failure, AICAR-mediated AMPK activation decreased IL-6 expression.

    In plain wordsIn mice, AMPK activation with AICAR reduced IL-6 expression during liver failure.

    Outcome
    DecreaseIL-6 expression
    Study

    mousen: not reported in source

    D-GalN/LPS-induced acute liver failure
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activation ameliorated ALF by inhibiting inflammation (downregulated TNF-α, IL-1β and IL-6 expression), activating autophagy (increased Atg-5, Beclin-1 and Atg-7 expression) and upregulating Foxo3A expression.
    1 context sentence
    Summary · context
    AMPK activation and inhibition of autophagy were induced by AICAR and 3-MA, respectively.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mice with acute liver failure, AICAR-mediated AMPK activation activated autophagy.

    In plain wordsIn mice, AMPK activation with AICAR increased autophagy during liver failure.

    Outcome
    IncreaseAutophagy
    Study

    mousen: not reported in source

    D-GalN/LPS-induced acute liver failure
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activation ameliorated ALF by inhibiting inflammation (downregulated TNF-α, IL-1β and IL-6 expression), activating autophagy (increased Atg-5, Beclin-1 and Atg-7 expression) and upregulating Foxo3A expression.
    1 context sentence
    Summary · context
    AMPK activation and inhibition of autophagy were induced by AICAR and 3-MA, respectively.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In mice with acute liver failure, AICAR-mediated AMPK activation increased Atg-5 expression.

    In plain wordsIn mice, AMPK activation with AICAR increased Atg-5 expression during liver failure.

    Outcome
    IncreaseAtg-5 expression
    Study

    mousen: not reported in source

    D-GalN/LPS-induced acute liver failure
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activation ameliorated ALF by inhibiting inflammation (downregulated TNF-α, IL-1β and IL-6 expression), activating autophagy (increased Atg-5, Beclin-1 and Atg-7 expression) and upregulating Foxo3A expression.
    1 context sentence
    Summary · context
    AMPK activation and inhibition of autophagy were induced by AICAR and 3-MA, respectively.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In mice with acute liver failure, AICAR-mediated AMPK activation increased Beclin-1 expression.

    In plain wordsIn mice, AMPK activation with AICAR increased Beclin-1 expression during liver failure.

    Outcome
    IncreaseBeclin-1 expression
    Study

    mousen: not reported in source

    D-GalN/LPS-induced acute liver failure
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activation ameliorated ALF by inhibiting inflammation (downregulated TNF-α, IL-1β and IL-6 expression), activating autophagy (increased Atg-5, Beclin-1 and Atg-7 expression) and upregulating Foxo3A expression.
    1 context sentence
    Summary · context
    AMPK activation and inhibition of autophagy were induced by AICAR and 3-MA, respectively.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In mice with acute liver failure, AICAR-mediated AMPK activation increased Atg-7 expression.

    In plain wordsIn mice, AMPK activation with AICAR increased Atg-7 expression during liver failure.

    Outcome
    IncreaseAtg-7 expression
    Study

    mousen: not reported in source

    D-GalN/LPS-induced acute liver failure
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activation ameliorated ALF by inhibiting inflammation (downregulated TNF-α, IL-1β and IL-6 expression), activating autophagy (increased Atg-5, Beclin-1 and Atg-7 expression) and upregulating Foxo3A expression.
    1 context sentence
    Summary · context
    AMPK activation and inhibition of autophagy were induced by AICAR and 3-MA, respectively.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In mice with acute liver failure, AICAR-mediated AMPK activation increased Foxo3A expression.

    In plain wordsIn mice, AMPK activation with AICAR increased Foxo3A expression during liver failure.

    Outcome
    IncreaseFoxo3A expression
    Study

    mousen: not reported in source

    D-GalN/LPS-induced acute liver failure
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activation ameliorated ALF by inhibiting inflammation (downregulated TNF-α, IL-1β and IL-6 expression), activating autophagy (increased Atg-5, Beclin-1 and Atg-7 expression) and upregulating Foxo3A expression.
    1 context sentence
    Summary · context
    AMPK activation and inhibition of autophagy were induced by AICAR and 3-MA, respectively.

Studies that did not test the peptide alone1

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. 10LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Efficacy outcome

    In hepatocytes, AMPK activation in the conditioned-medium experiment alleviated liver failure in vitro.

    In plain wordsIn cells, the experiment with conditioned medium from AICAR-treated macrophages reduced liver failure-related injury.

    Outcome
    DecreaseLiver failure in vitro
    Study

    n: not reported in source

    hepatocytes exposed to BMDM-conditioned medium
    Outcome group
    Liver fat and liver function · Liver

    Source sentences

    Summary
    In addition, AMPK activation alleviated liver failure in vitro.
    2 context sentences
    Summary · context
    Lastly, the BMDM-conditioned medium (BMDM-CM) derived from BMDMs treated with AICAR and LPS were used to explore the effect of AMPK and Foxo3A on hepatocytes.
    Summary · context
    AMPK activation and inhibition of autophagy were induced by AICAR and 3-MA, respectively.

    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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