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Study · Animal study (in vivo) · rat · 2026

5 results

Nicorandil ameliorates cardiac microcirculation in hypertensive myocardial infarction via LKB1/AMPK signaling activation.

Wang W, Wang S

Pakistan journal of pharmaceutical sciences1 Mar 2026

PMID41620890 (opens in a new tab)DOI10.36721/pjps.2026.39.3.reg.14441.1 (opens in a new tab)PepBankPUB-41620890
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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 study5

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In rats with hypertensive myocardial infarction, AICAR restored LKB1/AMPK signaling versus the model group.

    In plain wordsIn rats with hypertensive heart injury, AICAR restored LKB1/AMPK signaling compared with the model group.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseLKB1/AMPK signaling
    Study

    ratn: not reported in source

    Hypertensive myocardial infarction in spontaneously hypertensive rats
    Comparator
    HMI model group
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both pharmacological activation with AICAR and Nic treatment effectively restored LKB1/AMPK signaling, attenuated myocardial damage and significantly lowered oxidative stress and inflammatory markers (P<0.05 versus model group).
    1 context sentence
    Summary · context
    Using spontaneously hypertensive rats (SHRs) to establish HMI models, we allocated animals into four experimental groups: control, model (HMI modeling), activation (AICAR, a pharmacological LKB1/AMPK activator) and Nic groups (Nic intervention).
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In rats with hypertensive myocardial infarction, AICAR attenuated myocardial damage versus the model group.

    In plain wordsIn rats with hypertensive heart injury, AICAR reduced heart muscle damage compared with the model group.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseMyocardial damage
    Study

    ratn: not reported in source

    Hypertensive myocardial infarction in spontaneously hypertensive rats
    Comparator
    HMI model group
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both pharmacological activation with AICAR and Nic treatment effectively restored LKB1/AMPK signaling, attenuated myocardial damage and significantly lowered oxidative stress and inflammatory markers (P<0.05 versus model group).
    1 context sentence
    Summary · context
    Using spontaneously hypertensive rats (SHRs) to establish HMI models, we allocated animals into four experimental groups: control, model (HMI modeling), activation (AICAR, a pharmacological LKB1/AMPK activator) and Nic groups (Nic intervention).
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In rats with hypertensive myocardial infarction, AICAR significantly lowered oxidative stress markers versus the model group.

    In plain wordsIn rats with hypertensive heart injury, AICAR reduced oxidative stress markers compared with the model group.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseOxidative stress markers
    Study

    ratn: not reported in source

    Hypertensive myocardial infarction in spontaneously hypertensive rats
    Comparator
    HMI model group
    Outcome group
    Oxidative stress · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both pharmacological activation with AICAR and Nic treatment effectively restored LKB1/AMPK signaling, attenuated myocardial damage and significantly lowered oxidative stress and inflammatory markers (P<0.05 versus model group).
    1 context sentence
    Summary · context
    Using spontaneously hypertensive rats (SHRs) to establish HMI models, we allocated animals into four experimental groups: control, model (HMI modeling), activation (AICAR, a pharmacological LKB1/AMPK activator) and Nic groups (Nic intervention).
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In rats with hypertensive myocardial infarction, AICAR significantly lowered inflammatory markers versus the model group.

    In plain wordsIn rats with hypertensive heart injury, AICAR reduced inflammation markers compared with the model group.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseInflammatory markers
    Study

    ratn: not reported in source

    Hypertensive myocardial infarction in spontaneously hypertensive rats
    Comparator
    HMI model group
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Both pharmacological activation with AICAR and Nic treatment effectively restored LKB1/AMPK signaling, attenuated myocardial damage and significantly lowered oxidative stress and inflammatory markers (P<0.05 versus model group).
    1 context sentence
    Summary · context
    Using spontaneously hypertensive rats (SHRs) to establish HMI models, we allocated animals into four experimental groups: control, model (HMI modeling), activation (AICAR, a pharmacological LKB1/AMPK activator) and Nic groups (Nic intervention).
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In rats with hypertensive myocardial infarction, AICAR was less effective than nicorandil in ameliorating pathological changes.

    In plain wordsIn rats with hypertensive heart injury, AICAR improved pathological changes less than nicorandil.

    Peptide
    AICAR (acadesine)
    Outcome
    Direction not reportedPathological changes versus nicorandil
    Study

    ratn: not reported in source

    Hypertensive myocardial infarction in spontaneously hypertensive rats
    Comparator
    Nicorandil
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Importantly, Nic treatment demonstrated superior efficacy compared to AICAR intervention in ameliorating HMI-induced pathological changes.
    1 context sentence
    Summary · context
    Using spontaneously hypertensive rats (SHRs) to establish HMI models, we allocated animals into four experimental groups: control, model (HMI modeling), activation (AICAR, a pharmacological LKB1/AMPK activator) and Nic groups (Nic intervention).

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

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