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Study · Animal study (in vivo) · rat · 2018

9 results

κ-opioid receptor activation protects against myocardial ischemia-reperfusion injury via AMPK/Akt/eNOS signaling activation.

Zhang S, Zhou Y, Zhao L, Tian X, Jia M, Gu X, Feng N, An R, Yang L, Zheng G, Li J, Guo H, Fan R, Pei J

European journal of pharmacology30 May 2018Cited by 24 (Europe PMC)

PMID29856969 (opens in a new tab)DOI10.1016/j.ejphar.2018.05.043 (opens in a new tab)PepBankPUB-29856969
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 study9

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In rats with myocardial ischemia-reperfusion injury, AICAR mimicked the improvement in cardiac function from U50,488 H.

    In plain wordsIn rats with heart ischemia-reperfusion injury, AICAR mimicked the improvement in heart function from U50,488 H.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseCardiac function
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR, an AMPK activator, mimicked the effect of U50,488 H.
    2 context sentences
    Summary · context
    In vivo study showed that U50,488 H improved cardiac function, reduced myocardial infarct size and serum cTnT significantly.
    Summary · context
    Myocardial I/R rat model and simulated I/R cardiomyocytes model were established.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In rats with myocardial ischemia-reperfusion injury, AICAR mimicked the reduction in infarct size from U50,488 H.

    In plain wordsIn rats with heart ischemia-reperfusion injury, AICAR mimicked the reduction in infarct size from U50,488 H.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseMyocardial infarct size
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR, an AMPK activator, mimicked the effect of U50,488 H.
    2 context sentences
    Summary · context
    In vivo study showed that U50,488 H improved cardiac function, reduced myocardial infarct size and serum cTnT significantly.
    Summary · context
    Myocardial I/R rat model and simulated I/R cardiomyocytes model were established.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In rats with myocardial ischemia-reperfusion injury, AICAR mimicked the reduction in serum cTnT from U50,488 H.

    In plain wordsIn rats with heart ischemia-reperfusion injury, AICAR mimicked the reduction in serum cTnT from U50,488 H.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseSerum cTnT
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR, an AMPK activator, mimicked the effect of U50,488 H.
    2 context sentences
    Summary · context
    In vivo study showed that U50,488 H improved cardiac function, reduced myocardial infarct size and serum cTnT significantly.
    Summary · context
    Myocardial I/R rat model and simulated I/R cardiomyocytes model were established.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In rats with myocardial ischemia-reperfusion injury, AICAR increased p-Akt, and Compound C abolished this effect.

    In plain wordsIn rats, AICAR increased Akt phosphorylation, and Compound C blocked this effect.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseAkt phosphorylation in vivo
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR increased p-Akt and p-eNOS, which was abolished by Compound C.
    1 context sentence
    Summary · context
    Myocardial I/R rat model and simulated I/R cardiomyocytes model were established.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In rats with myocardial ischemia-reperfusion injury, AICAR increased p-eNOS, and Compound C abolished this effect.

    In plain wordsIn rats, AICAR increased eNOS phosphorylation, and Compound C blocked this effect.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseeNOS phosphorylation in vivo
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR increased p-Akt and p-eNOS, which was abolished by Compound C.
    1 context sentence
    Summary · context
    Myocardial I/R rat model and simulated I/R cardiomyocytes model were established.
  6. 06LabIn vitro (cells)Mechanism

    In cardiomyocytes, AICAR increased p-Akt, which Akt inhibition but not L-NAME abolished.

    In plain wordsIn cells, AICAR increased Akt phosphorylation, which an Akt inhibitor blocked but L-NAME did not.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseAkt phosphorylation in vitro
    Study

    n: not reported in source

    Cardiomyocytes subjected to simulated ischemia-reperfusion
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR increased p-Akt and p-eNOS, which was abolished by Akt inhibitor, but not L-NAME.
    1 context sentence
    Summary · context
    Myocardial I/R rat model and simulated I/R cardiomyocytes model were established.
  7. 07LabIn vitro (cells)Mechanism

    In cardiomyocytes, AICAR increased p-eNOS, which Akt inhibition but not L-NAME abolished.

    In plain wordsIn cells, AICAR increased eNOS phosphorylation, which an Akt inhibitor blocked but L-NAME did not.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseeNOS phosphorylation in vitro
    Study

    n: not reported in source

    Cardiomyocytes subjected to simulated ischemia-reperfusion
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR increased p-Akt and p-eNOS, which was abolished by Akt inhibitor, but not L-NAME.
    1 context sentence
    Summary · context
    Myocardial I/R rat model and simulated I/R cardiomyocytes model were established.
  8. 08LabIn vitro (cells)Efficacy outcome

    In cardiomyocytes subjected to simulated ischemia-reperfusion, AICAR increased viability.

    In plain wordsIn cells subjected to simulated ischemia-reperfusion, AICAR increased survival.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseCardiomyocyte viability
    Study

    n: not reported in source

    Cardiomyocytes subjected to simulated ischemia-reperfusion
    Outcome group
    Cell viability and death · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    U50,488 H and AICAR also increased the viability of cardiomyocytes subjected to simulated I/R, the effects of U50,488 H and AICAR were blocked by nor-BNI, Compound C, Akt inhibitor, and L-NAME, respectively.
    1 context sentence
    Summary · context
    Myocardial I/R rat model and simulated I/R cardiomyocytes model were established.

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. 09LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In cardiomyocytes under simulated ischemia-reperfusion, the reported inhibitors blocked the viability effects of U50,488 H and AICAR.

    In plain wordsIn cells under simulated ischemia-reperfusion, the reported inhibitors blocked the survival effects of U50,488 H and AICAR.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseInhibitor blockade of AICAR-associated cardiomyocyte viability
    Study

    n: not reported in source

    Cardiomyocytes subjected to simulated ischemia-reperfusion
    Outcome group
    Cell viability and death · Cardiovascular

    Source sentences

    Summary
    U50,488 H and AICAR also increased the viability of cardiomyocytes subjected to simulated I/R, the effects of U50,488 H and AICAR were blocked by nor-BNI, Compound C, Akt inhibitor, and L-NAME, 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.

Publication types

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