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Study · In vitro (cells) · mouse · 2001

5 results

Hexarelin protects H9c2 cardiomyocytes from doxorubicin-induced cell death.

Filigheddu N, Fubini A, Baldanzi G, Cutrupi S, Ghè C, Catapano F, Broglio F, Bosia A, Papotti M, Muccioli G, Ghigo E, Deghenghi R, Graziani A

Endocrine1 Feb 2001Cited by 29 (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 study5

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

  1. 01LabIn vitro (cells)Activity measurement

    In H9c2 cardiomyocytes, hexarelin inhibited specific binding of labelled Tyr-Ala-hexarelin, whereas the nonpeptidyl GHS MK-0677 did not.

    In plain wordsIn cells, hexarelin blocked the binding of a labelled hexarelin analogue to heart cells, but the drug MK-0677 did not.

    Peptide
    Hexarelin
    Outcome
    DecreaseCompetition for 125I-Tyr-Ala-hexarelin binding in H9c2 cardiomyocytes
    Study

    n: not reported in source

    H9c2 cardiomyocytes
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    H9c2 cardiomyocytes show specific binding for 125I-Tyr-Ala-hexarelin, which is inhibited by peptidyl GHSs such as Tyr-Ala-hexarelin and hexarelin but not by the nonpeptidyl GHS MK-0677
    1 context sentence
    Summary · context
    To verify the hypothesis that peptidyl GHSs protect heart cells from cell death, we have investigated the cellular effects of hexarelin on H9c2 cardiomyocytes, a fetal cardiomyocyte-derived cell line, and on Hend, an endothelial cell line derived from transformed murine heart endothelium.
  2. 02LabIn vitro (cells)Efficacy outcome

    Hexarelin promoted survival of H9c2 cardiomyocytes induced to die by doxorubicin.

    In plain wordsIn cells, hexarelin helped heart cells survive doxorubicin, a drug that kills them.

    Peptide
    Hexarelin
    Outcome
    IncreaseSurvival of H9c2 cardiomyocytes exposed to doxorubicin
    Study

    n: not reported in source

    H9c2 cardiomyocytes with doxorubicin
    Outcome group
    Myocardial injury · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    hexarelin promotes survival of H9c2 cardiomyocytes induced to die by doxorubicin
    1 context sentence
    Summary · context
    To verify the hypothesis that peptidyl GHSs protect heart cells from cell death, we have investigated the cellular effects of hexarelin on H9c2 cardiomyocytes, a fetal cardiomyocyte-derived cell line, and on Hend, an endothelial cell line derived from transformed murine heart endothelium.
  3. 03LabIn vitro (cells)Efficacy outcome

    Hexarelin inhibited apoptosis, measured by DNA fragmentation, in H9c2 myocytes.

    In plain wordsIn cells, hexarelin reduced programmed cell death in heart muscle cells.

    Peptide
    Hexarelin
    Outcome
    DecreaseApoptosis (DNA fragmentation) in H9c2 cardiomyocytes
    Study

    n: not reported in source

    H9c2 cardiomyocytes with doxorubicin
    Outcome group
    Myocardial injury · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    hexarelin inhibits apoptosis, as measured by DNA fragmentation, induced in both H9c2 myocytes and endothelial cells
    1 context sentence
    Summary · context
    To verify the hypothesis that peptidyl GHSs protect heart cells from cell death, we have investigated the cellular effects of hexarelin on H9c2 cardiomyocytes, a fetal cardiomyocyte-derived cell line, and on Hend, an endothelial cell line derived from transformed murine heart endothelium.
  4. 04LabIn vitro (cells)Efficacy outcome

    Hexarelin inhibited apoptosis, measured by DNA fragmentation, in Hend endothelial cells.

    In plain wordsIn cells, hexarelin reduced programmed cell death in mouse heart blood-vessel lining cells.

    Peptide
    Hexarelin
    Outcome
    DecreaseApoptosis (DNA fragmentation) in Hend endothelial cells
    Study

    mousen: not reported in source

    Hend murine heart endothelial cells
    Outcome group
    Myocardial injury · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    hexarelin inhibits apoptosis, as measured by DNA fragmentation, induced in both H9c2 myocytes and endothelial cells
    1 context sentence
    Summary · context
    To verify the hypothesis that peptidyl GHSs protect heart cells from cell death, we have investigated the cellular effects of hexarelin on H9c2 cardiomyocytes, a fetal cardiomyocyte-derived cell line, and on Hend, an endothelial cell line derived from transformed murine heart endothelium.
  5. 05LabIn vitro (cells)Activity measurement

    In H9c2 cardiomyocytes, MK-0677 did not inhibit specific binding of radiolabeled Tyr-Ala-hexarelin.

    In plain wordsIn cells, MK-0677 did not block labeled hexarelin binding.

    Outcome
    No significant changeRadioligand binding displacement
    Study

    n: not reported in source

    H9c2 cardiomyocytes
    Outcome group
    Receptor activity and mechanism · Pharmacology
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We show that (i)H9c2 cardiomyocytes show specific binding for 125I-Tyr-Ala-hexarelin, which is inhibited by peptidyl GHSs such as Tyr-Ala-hexarelin and hexarelin but not by the nonpeptidyl GHS MK-0677

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 3Current

    14 Oct 2026, 01:46 UTC

    Study data updated · source update from Europe PMC

  2. Version 2

    13 Oct 2026, 21:44 UTC

    Study results updated

  3. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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