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Study · In vitro (cells) · 2021

7 results

AICAR Protects Vascular Endothelial Cells from Oxidative Injury Induced by the Long-Term Palmitate Excess.

Samsonov MV, Podkuychenko NV, Khapchaev AY, Efremov EE, Yanushevskaya EV, Vlasik TN, Lankin VZ, Stafeev IS, Skulachev MV, Shestakova MV, Vorotnikov AV, Shirinsky VP

International journal of molecular sciences25 Dec 2021Cited by 22 (Europe PMC)

PMID35008640 (opens in a new tab)PMCIDPMC8745318 (opens in a new tab)DOI10.3390/ijms23010211 (opens in a new tab)PepBankPUB-35008640
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Summary

Hyperlipidemia manifested by high blood levels of free fatty acids (FFA) and lipoprotein triglycerides is critical for the progression of type 2 diabetes (T2D) and its cardiovascular complications via vascular endothelial dysfunction. However, attempts to assess high FFA effects in endothelial culture often result in early cell apoptosis that poorly recapitulates a much slower pace of vascular deterioration in vivo and does not provide for the longer-term studies of endothelial lipotoxicity in vitro. Here, we report that palmitate (PA), a typical FFA, does not impair, by itself, endothelial barrier and insulin signaling in human umbilical vein endothelial cells (HUVEC), but increases NO release, reactive oxygen species (ROS) generation, and protein labeling by malondialdehyde (MDA) hallmarking oxidative stress and increased lipid peroxidation. This PA-induced stress eventually resulted in the loss of cell viability coincident with loss of insulin signaling. Supplementation with 5-aminoimidazole-4-carboxamide-riboside (AICAR) increased endothelial AMP-activated protein kinase (AMPK) activity, supported insulin signaling, and prevented the PA-induced increases in NO, ROS, and MDA, thus allowing to maintain HUVEC viability and barrier, and providing the means to study the long-term effects of high FFA levels in endothelial cultures. An upgraded cell-based model reproduces FFA-induced insulin resistance by demonstrating decreased NO production by vascular endothelium.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study7

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

  1. 01LabIn vitro (cells)Mechanism

    In palmitate-exposed HUVEC, AICAR increased AMPK activity.

    In plain wordsIn cells, AICAR increased AMPK activity during palmitate exposure.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseAMPK activity
    Study

    humann: not reported in source

    palmitate-exposed HUVEC
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Supplementation with 5-aminoimidazole-4-carboxamide-riboside (AICAR) increased endothelial AMP-activated protein kinase (AMPK) activity,
  2. 02LabIn vitro (cells)Mechanism

    In palmitate-exposed HUVEC, AICAR supported insulin signaling.

    In plain wordsIn cells, AICAR supported insulin signaling during palmitate exposure.

    Peptide
    AICAR (acadesine)
    Outcome
    Direction not reportedInsulin signaling
    Study

    humann: not reported in source

    palmitate-exposed HUVEC
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Supplementation with 5-aminoimidazole-4-carboxamide-riboside (AICAR) increased endothelial AMP-activated protein kinase (AMPK) activity, supported insulin signaling,
  3. 03LabIn vitro (cells)Mechanism

    In HUVEC, AICAR prevented the palmitate-induced increase in NO.

    In plain wordsIn cells, AICAR prevented the palmitate-induced increase in nitric oxide.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseNO increase
    Study

    humann: not reported in source

    palmitate-exposed HUVEC
    Outcome group
    Oxidative stress · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Supplementation with 5-aminoimidazole-4-carboxamide-riboside (AICAR) increased endothelial AMP-activated protein kinase (AMPK) activity, supported insulin signaling, and prevented the PA-induced increases in NO, ROS, and MDA,
  4. 04LabIn vitro (cells)Mechanism

    In HUVEC, AICAR prevented the palmitate-induced increase in ROS.

    In plain wordsIn cells, AICAR prevented the palmitate-induced increase in reactive oxygen species.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseROS increase
    Study

    humann: not reported in source

    palmitate-exposed HUVEC
    Outcome group
    Oxidative stress · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Supplementation with 5-aminoimidazole-4-carboxamide-riboside (AICAR) increased endothelial AMP-activated protein kinase (AMPK) activity, supported insulin signaling, and prevented the PA-induced increases in NO, ROS, and MDA,
  5. 05LabIn vitro (cells)Mechanism

    In HUVEC, AICAR prevented the palmitate-induced increase in MDA.

    In plain wordsIn cells, AICAR prevented the palmitate-induced increase in MDA.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseMDA increase
    Study

    humann: not reported in source

    palmitate-exposed HUVEC
    Outcome group
    Oxidative stress · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Supplementation with 5-aminoimidazole-4-carboxamide-riboside (AICAR) increased endothelial AMP-activated protein kinase (AMPK) activity, supported insulin signaling, and prevented the PA-induced increases in NO, ROS, and MDA,
  6. 06LabIn vitro (cells)Efficacy outcome

    In palmitate-exposed HUVEC, AICAR allowed maintenance of cell viability.

    In plain wordsIn cells, AICAR preserved viability during palmitate exposure.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseCell viability
    Study

    humann: not reported in source

    palmitate-exposed HUVEC
    Outcome group
    Cell viability and death · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Supplementation with 5-aminoimidazole-4-carboxamide-riboside (AICAR) increased endothelial AMP-activated protein kinase (AMPK) activity, supported insulin signaling, and prevented the PA-induced increases in NO, ROS, and MDA, thus allowing to maintain HUVEC viability and barrier,
  7. 07LabIn vitro (cells)Efficacy outcome

    In palmitate-exposed HUVEC, AICAR allowed maintenance of the endothelial barrier.

    In plain wordsIn cells, AICAR preserved the endothelial barrier during palmitate exposure.

    Peptide
    AICAR (acadesine)
    Outcome
    Direction not reportedEndothelial barrier
    Study

    humann: not reported in source

    palmitate-exposed HUVEC
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Supplementation with 5-aminoimidazole-4-carboxamide-riboside (AICAR) increased endothelial AMP-activated protein kinase (AMPK) activity, supported insulin signaling, and prevented the PA-induced increases in NO, ROS, and MDA, thus allowing to maintain HUVEC viability and barrier,

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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