Skip to content

Study · Animal study (in vivo) · mouse · 2004

8 results

MC-3 receptor and the inflammatory mechanisms activated in acute myocardial infarct.

Getting SJ, Di Filippo C, Christian HC, Lam CW, Rossi F, D'Amico M, Perretti M

Journal of leukocyte biology26 Jul 2004Cited by 35 (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 study8

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice, MTII given 30 min before ischemia attenuated heart reperfusion injury at 2 h by approximately 40%.

    In plain wordsIn mice, MTII given before blood flow stopped reduced heart injury after blood flow returned by about 40%.

    Outcome
    DecreaseHeart reperfusion injury at 2 h (MTII before ischemia)
    Study

    mousen: not reported in source

    Mouse myocardial ischemia-reperfusion injury
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    10 µg per mouseAs given in this study (mouse).

    Measurements

    Reduction in reperfusion injury
    ≈ 40%
    2 h reperfusion

    Source sentences

    Summary
    administration of the melanocortin agonist MTII (10 microg per mouse equivalent to 9.3 nmol) 30 min prior to ischemia (25 min) attenuated mouse heart 2 h reperfusion injury by approximately 40%
    1 context sentence
    Summary · context
    Here we exploited the potential protective role that melanocortin receptor type 3 (MC3-R) activation might play in a myocardial ischemia-reperfusion injury model.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mice, the cardioprotective effect of MTII was prevented by the mixed MC3/4-R antagonist SHU9119 but not by the selective MC4-R antagonist HS204.

    In plain wordsIn mice, the heart protection from MTII was blocked by a drug acting on MC3 and MC4 receptors, but not by an MC4-only blocker.

    Outcome
    Not applicableReceptor dependence of MTII cardioprotection
    Study

    mousen: not reported in source

    Mouse myocardial ischemia-reperfusion injury
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    10 µg per mouseAs given in this study (mouse).

    Source sentences

    Summary
    an effect prevented by the mixed MC3/4-R antagonist SHU9119 but not by the selective MC4-R antagonist HS204.
    1 context sentence
    Summary · context
    Here we exploited the potential protective role that melanocortin receptor type 3 (MC3-R) activation might play in a myocardial ischemia-reperfusion injury model.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice, MTII given at the beginning of reperfusion gave similar protection against heart reperfusion injury.

    In plain wordsIn mice, MTII given when blood flow returned also protected the heart from injury.

    Outcome
    DecreaseHeart reperfusion injury (MTII at start of reperfusion)
    Study

    mousen: not reported in source

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

    Source sentences

    Summary
    Similar results were obtained when the compound was given at the beginning of the reperfusion period.
    1 context sentence
    Summary · context
    Here we exploited the potential protective role that melanocortin receptor type 3 (MC3-R) activation might play in a myocardial ischemia-reperfusion injury model.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mice, 10 µg MTII equally protected against delayed myocardial damage measured 24 h after reperfusion.

    In plain wordsIn mice, MTII also protected the heart from damage that appeared 24 hours after blood flow returned.

    Outcome
    DecreaseDelayed myocardial damage at 24 h post-reperfusion
    Study

    mousen: not reported in source

    Mouse myocardial ischemia-reperfusion injury
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    10 µg per mouseAs given in this study (mouse).

    Source sentences

    Summary
    Importantly, delayed myocardial damage as measured 24 h post-reperfusion was equally protected by administration of 10 microg MTII.
    1 context sentence
    Summary · context
    Here we exploited the potential protective role that melanocortin receptor type 3 (MC3-R) activation might play in a myocardial ischemia-reperfusion injury model.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In recessive yellow (e/e) mice with a mutated, inactive MC1-R, MTII was fully protective against heart reperfusion injury.

    In plain wordsIn mice with an inactive MC1 receptor, MTII still fully protected the heart from injury.

    Outcome
    DecreaseCardioprotection in recessive yellow (e/e) mice with inactive MC1-R
    Study

    mousen: not reported in source

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

    Source sentences

    Summary
    The focus on MC3-R was also substantiated by analysis of the recessive yellow (e/e) mouse, bearing a mutated (inactive) MC1-R, in which MTII was fully protective.
    1 context sentence
    Summary · context
    Here we exploited the potential protective role that melanocortin receptor type 3 (MC3-R) activation might play in a myocardial ischemia-reperfusion injury model.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In mice, myocardial protection by MTII coincided with reduced interleukin-1 content.

    In plain wordsIn mice, heart protection by MTII coincided with lower interleukin-1, a marker of inflammation.

    Outcome
    DecreaseInterleukin-1 content
    Study

    mousen: not reported in source

    Mouse myocardial ischemia-reperfusion injury
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Myocardial protection was associated with reduced markers of systemic and local inflammation, including cytokine contents (interleukin-1 and KC) and myeloperoxidase activity.
    1 context sentence
    Summary · context
    Here we exploited the potential protective role that melanocortin receptor type 3 (MC3-R) activation might play in a myocardial ischemia-reperfusion injury model.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In mice, myocardial protection by MTII coincided with reduced KC cytokine content.

    In plain wordsIn mice, heart protection by MTII coincided with lower KC, a marker of inflammation.

    Outcome
    DecreaseKC (chemokine) content
    Study

    mousen: not reported in source

    Mouse myocardial ischemia-reperfusion injury
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Myocardial protection was associated with reduced markers of systemic and local inflammation, including cytokine contents (interleukin-1 and KC) and myeloperoxidase activity.
    1 context sentence
    Summary · context
    Here we exploited the potential protective role that melanocortin receptor type 3 (MC3-R) activation might play in a myocardial ischemia-reperfusion injury model.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In mice, myocardial protection by MTII coincided with reduced myeloperoxidase activity.

    In plain wordsIn mice, heart protection by MTII coincided with lower myeloperoxidase activity, a marker of inflammation.

    Outcome
    DecreaseMyeloperoxidase activity
    Study

    mousen: not reported in source

    Mouse myocardial ischemia-reperfusion injury
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Myocardial protection was associated with reduced markers of systemic and local inflammation, including cytokine contents (interleukin-1 and KC) and myeloperoxidase activity.
    1 context sentence
    Summary · context
    Here we exploited the potential protective role that melanocortin receptor type 3 (MC3-R) activation might play in a myocardial ischemia-reperfusion injury model.

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

    10 Oct 2026, 09:43 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.