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Study · Animal study (in vivo) · mouse · 2008

10 results

Activation of AMPK attenuates neutrophil proinflammatory activity and decreases the severity of acute lung injury.

Zhao X, Zmijewski JW, Lorne E, Liu G, Park YJ, Tsuruta Y, Abraham E

American journal of physiology. Lung cellular and molecular physiology27 Jun 2008Cited by 259 (Europe PMC)

PMID18586954 (opens in a new tab)PMCIDPMC2536800 (opens in a new tab)DOI10.1152/ajplung.90210.2008 (opens in a new tab)PepBankPUB-18586954
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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 study10

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In mice, AICAR administration activated lung AMPK.

    In plain wordsIn mice, AICAR activated AMPK in the lungs.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseLung AMPK activation
    Study

    mousen: not reported in source

    LPS-induced lung injury
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of AICAR to mice resulted in activation of AMPK in the lungs and was associated with decreased severity of LPS-induced lung injury, as determined by diminished neutrophil accumulation in the lungs, reduced interstitial pulmonary edema, and diminished levels of TNF-alpha and IL-6 in br…
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mice with LPS-induced lung injury, AICAR administration was associated with diminished lung neutrophil accumulation.

    In plain wordsIn mice with LPS-induced lung injury, AICAR was linked to fewer neutrophils in the lungs.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseLung neutrophil accumulation
    Study

    mousen: not reported in source

    LPS-induced lung injury
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of AICAR to mice resulted in activation of AMPK in the lungs and was associated with decreased severity of LPS-induced lung injury, as determined by diminished neutrophil accumulation in the lungs, reduced interstitial pulmonary edema, and diminished levels of TNF-alpha and IL-6 in br…
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mice with LPS-induced lung injury, AICAR administration was associated with reduced interstitial pulmonary edema.

    In plain wordsIn mice with LPS-induced lung injury, AICAR was linked to less fluid in lung tissue.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseInterstitial pulmonary edema
    Study

    mousen: not reported in source

    LPS-induced lung injury
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of AICAR to mice resulted in activation of AMPK in the lungs and was associated with decreased severity of LPS-induced lung injury, as determined by diminished neutrophil accumulation in the lungs, reduced interstitial pulmonary edema, and diminished levels of TNF-alpha and IL-6 in br…
  4. 04AnimalAnimal study (in vivo)Mechanism

    In mice with LPS-induced lung injury, AICAR administration was associated with diminished bronchoalveolar lavage TNF-alpha levels.

    In plain wordsIn mice with LPS-induced lung injury, AICAR was linked to lower TNF-alpha levels in lung wash fluid.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseBronchoalveolar TNF-alpha
    Study

    mousen: not reported in source

    LPS-induced lung injury
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of AICAR to mice resulted in activation of AMPK in the lungs and was associated with decreased severity of LPS-induced lung injury, as determined by diminished neutrophil accumulation in the lungs, reduced interstitial pulmonary edema, and diminished levels of TNF-alpha and IL-6 in br…
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mice with LPS-induced lung injury, AICAR administration was associated with diminished bronchoalveolar lavage IL-6 levels.

    In plain wordsIn mice with LPS-induced lung injury, AICAR was linked to lower IL-6 levels in lung wash fluid.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseBronchoalveolar IL-6
    Study

    mousen: not reported in source

    LPS-induced lung injury
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of AICAR to mice resulted in activation of AMPK in the lungs and was associated with decreased severity of LPS-induced lung injury, as determined by diminished neutrophil accumulation in the lungs, reduced interstitial pulmonary edema, and diminished levels of TNF-alpha and IL-6 in br…
  6. 06LabIn vitro (cells)Mechanism

    In murine bone marrow neutrophils, AICAR activated AMPK dose dependently.

    In plain wordsIn cells from mouse bone marrow, AICAR activated AMPK in a dose-dependent manner.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseAMPK activation
    Study

    mousen: not reported in source

    murine bone marrow neutrophils
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR and barberine dose-dependently activated AMPK in murine bone marrow neutrophils.
  7. 07LabIn vitro (cells)Mechanism

    In LPS-stimulated neutrophils, AICAR inhibited TNF-alpha release compared with LPS alone.

    In plain wordsIn cells stimulated with LPS, AICAR reduced TNF-alpha release compared with LPS alone.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseTNF-alpha release
    Study

    mousen: not reported in source

    LPS-stimulated neutrophils
    Comparator
    LPS without AICAR
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exposure of LPS-stimulated neutrophils to AICAR or barberine inhibited release of TNF-alpha and IL-6, as well as degradation of IkappaBalpha and nuclear translocation of NF-kappaB, compared with findings in neutrophil cultures that contained LPS without AICAR or barberine.
  8. 08LabIn vitro (cells)Mechanism

    In LPS-stimulated neutrophils, AICAR inhibited IL-6 release compared with LPS alone.

    In plain wordsIn cells stimulated with LPS, AICAR reduced IL-6 release compared with LPS alone.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseIL-6 release
    Study

    mousen: not reported in source

    LPS-stimulated neutrophils
    Comparator
    LPS without AICAR
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exposure of LPS-stimulated neutrophils to AICAR or barberine inhibited release of TNF-alpha and IL-6, as well as degradation of IkappaBalpha and nuclear translocation of NF-kappaB, compared with findings in neutrophil cultures that contained LPS without AICAR or barberine.
  9. 09LabIn vitro (cells)Mechanism

    In LPS-stimulated neutrophils, AICAR inhibited IkappaBalpha degradation compared with LPS alone.

    In plain wordsIn cells stimulated with LPS, AICAR reduced IkappaBalpha breakdown compared with LPS alone.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseIkappaBalpha degradation
    Study

    mousen: not reported in source

    LPS-stimulated neutrophils
    Comparator
    LPS without AICAR
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exposure of LPS-stimulated neutrophils to AICAR or barberine inhibited release of TNF-alpha and IL-6, as well as degradation of IkappaBalpha and nuclear translocation of NF-kappaB, compared with findings in neutrophil cultures that contained LPS without AICAR or barberine.
  10. 10LabIn vitro (cells)Mechanism

    In LPS-stimulated neutrophils, AICAR inhibited NF-kappaB nuclear translocation compared with LPS alone.

    In plain wordsIn cells stimulated with LPS, AICAR reduced NF-kappaB movement into the nucleus compared with LPS alone.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseNF-kappaB nuclear translocation
    Study

    mousen: not reported in source

    LPS-stimulated neutrophils
    Comparator
    LPS without AICAR
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exposure of LPS-stimulated neutrophils to AICAR or barberine inhibited release of TNF-alpha and IL-6, as well as degradation of IkappaBalpha and nuclear translocation of NF-kappaB, compared with findings in neutrophil cultures that contained LPS without AICAR or barberine.

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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