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

18 results

Combined Therapy with SS31 and Mitochondria Mitigates Myocardial Ischemia-Reperfusion Injury in Rats.

Lee FY, Shao PL, Wallace CG, Chua S, Sung PH, Ko SF, Chai HT, Chung SY, Chen KH, Lu HI, Chen YL, Huang TH, Sheu JJ, Yip HK

International journal of molecular sciences15 Sept 2018Cited by 58 (Europe PMC)

Summary

Myocardial ischemia-reperfusion (IR) injury contributes to adverse cardiac outcomes after myocardial ischemia, cardiac surgery, or circulatory arrest. In this study, we evaluated the ability of combined SS31-mitochondria (Mito) therapy to protect heart cells from myocardial IR injury. Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria). In H9C2 cells, SS31 suppressed menadione-induced oxidative-stress markers (NOX-1, NOX-2, oxidized protein) while it increased SIRT1/SIRT3 expression and ATP levels. In adult male rats 72 h after IR, left ventricular ejection fraction (LVEF) was highest in sham-operated control animals and lowest in the IR group. LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone. Areas of fibrosis/collagen-deposition showed the opposite pattern. Likewise, levels of oxidative-stress markers (NOX-1, NOX-2, oxidized protein), inflammatory markers (MMP-9, CD11, IL-1β, TNF-α), apoptotic markers (mitochondrial-Bax, cleaved-caspase-3, PARP), fibrosis markers (p-Smad3, TGF-β), DNA-damage (γ-H2AX), sarcomere-length, and pressure/volume overload markers (BNP, β-MHC) all showed a pattern opposite that of LVEF. Conversely, anti-apoptotic (BMP-2, Smad1/5) and energy integrity (PGC-1α/mitochondrial cytochrome-C) markers exhibited a pattern identical to that of LVEF. This study demonstrates that the combined SS31-Mito therapy is superior to either therapy alone for protecting myocardium from IR injury and indicates that the responsible mechanisms involved increased SIRT1/SIRT3 expression, which suppresses inflammation and oxidative stress and protects mitochondrial integrity.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study18

6 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, combined SS31-Mito therapy gave a higher left ventricular ejection fraction than Mito alone.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave better heart pumping than mitochondria alone.

    Outcome
    IncreaseLeft ventricular ejection fraction, SS31-Mito versus Mito alone
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    Mito alone
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    2 mg · intraperitoneal · 30 min, 24 h and 48 h after IR; assessed at 72 hAs given in this study (rat).

    Source sentences

    Summary
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    1 context sentence
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).
  2. 02LabIn vitro (cells)Mechanism

    In H9C2 cells, SS31 suppressed the menadione-induced oxidative-stress marker NOX-1.

    In plain wordsIn heart cells, SS31 lowered the oxidative-stress marker NOX-1 caused by menadione.

    Outcome
    DecreaseNOX-1 expression in H9C2 cells
    Study

    ratn: not reported in source

    H9C2 cells with menadione-induced oxidative stress
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In H9C2 cells, SS31 suppressed menadione-induced oxidative-stress markers (NOX-1, NOX-2, oxidized protein) while it increased SIRT1/SIRT3 expression and ATP levels.
  3. 03LabIn vitro (cells)Mechanism

    In H9C2 cells, SS31 suppressed the menadione-induced oxidative-stress marker NOX-2.

    In plain wordsIn heart cells, SS31 lowered the oxidative-stress marker NOX-2 caused by menadione.

    Outcome
    DecreaseNOX-2 expression in H9C2 cells
    Study

    ratn: not reported in source

    H9C2 cells with menadione-induced oxidative stress
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In H9C2 cells, SS31 suppressed menadione-induced oxidative-stress markers (NOX-1, NOX-2, oxidized protein) while it increased SIRT1/SIRT3 expression and ATP levels.
  4. 04LabIn vitro (cells)Mechanism

    In H9C2 cells, SS31 suppressed the menadione-induced oxidative-stress marker oxidized protein.

    In plain wordsIn heart cells, SS31 lowered the level of oxidized protein caused by menadione.

    Outcome
    DecreaseOxidized protein in H9C2 cells
    Study

    ratn: not reported in source

    H9C2 cells with menadione-induced oxidative stress
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In H9C2 cells, SS31 suppressed menadione-induced oxidative-stress markers (NOX-1, NOX-2, oxidized protein) while it increased SIRT1/SIRT3 expression and ATP levels.
  5. 05LabIn vitro (cells)Mechanism

    In H9C2 cells, SS31 increased SIRT1 and SIRT3 expression.

    In plain wordsIn heart cells, SS31 raised the levels of the proteins SIRT1 and SIRT3.

    Outcome
    IncreaseSIRT1/SIRT3 expression in H9C2 cells
    Study

    ratn: not reported in source

    H9C2 cells with menadione-induced oxidative stress
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In H9C2 cells, SS31 suppressed menadione-induced oxidative-stress markers (NOX-1, NOX-2, oxidized protein) while it increased SIRT1/SIRT3 expression and ATP levels.
  6. 06LabIn vitro (cells)Mechanism

    In H9C2 cells, SS31 increased ATP levels.

    In plain wordsIn heart cells, SS31 raised ATP (cell energy) levels.

    Outcome
    IncreaseATP level in H9C2 cells
    Study

    ratn: not reported in source

    H9C2 cells with menadione-induced oxidative stress
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In H9C2 cells, SS31 suppressed menadione-induced oxidative-stress markers (NOX-1, NOX-2, oxidized protein) while it increased SIRT1/SIRT3 expression and ATP levels.

Studies that did not test the peptide alone12

In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  1. 07AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Efficacy outcome

    In rats with myocardial ischemia-reperfusion injury, combined SS31-Mito therapy gave a higher left ventricular ejection fraction than no treatment.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave better heart pumping than no treatment.

    Outcome
    IncreaseLeft ventricular ejection fraction, SS31-Mito versus untreated IR
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    Untreated IR
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    2 context sentences
    Summary · context
    In adult male rats 72 h after IR, left ventricular ejection fraction (LVEF) was highest in sham-operated control animals and lowest in the IR group.
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  2. 08AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Efficacy outcome

    In rats with myocardial ischemia-reperfusion injury, combined SS31-Mito therapy gave a higher left ventricular ejection fraction than SS31 alone.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave better heart pumping than SS31 alone.

    Outcome
    IncreaseLeft ventricular ejection fraction, SS31-Mito versus SS31 alone
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    SS31 alone
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    1 context sentence
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  3. 09AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Efficacy outcome

    In rats with myocardial ischemia-reperfusion injury, areas of fibrosis and collagen deposition showed the opposite pattern to ejection fraction, so they were smaller with SS31-Mito.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave less scarring than the other IR groups.

    Outcome
    DecreaseFibrosis and collagen deposition
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    Other IR groups (untreated, Mito alone, SS31 alone)
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    Areas of fibrosis/collagen-deposition showed the opposite pattern.
    2 context sentences
    Summary · context
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  4. 10AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism

    In rats with myocardial ischemia-reperfusion injury, oxidative-stress markers showed a pattern opposite to ejection fraction, so they were lowest with SS31-Mito among the IR groups.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave lower oxidative-stress markers than the other IR groups.

    Outcome
    DecreaseOxidative-stress markers (NOX-1, NOX-2, oxidized protein)
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    Other IR groups (untreated, Mito alone, SS31 alone)
    Outcome group
    Inflammation markers · Cardiovascular

    Source sentences

    Summary
    Likewise, levels of oxidative-stress markers (NOX-1, NOX-2, oxidized protein)
    3 context sentences
    Summary · context
    all showed a pattern opposite that of LVEF.
    Summary · context
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  5. 11AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism

    In rats with myocardial ischemia-reperfusion injury, inflammatory markers showed a pattern opposite to ejection fraction, so they were lowest with SS31-Mito among the IR groups.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave lower inflammation markers than the other IR groups.

    Outcome
    DecreaseInflammatory markers (MMP-9, CD11, IL-1β, TNF-α)
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    Other IR groups (untreated, Mito alone, SS31 alone)
    Outcome group
    Inflammation markers · Cardiovascular

    Source sentences

    Summary
    inflammatory markers (MMP-9, CD11, IL-1β, TNF-α)
    3 context sentences
    Summary · context
    all showed a pattern opposite that of LVEF.
    Summary · context
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  6. 12AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism

    In rats with myocardial ischemia-reperfusion injury, apoptotic markers showed a pattern opposite to ejection fraction, so they were lowest with SS31-Mito among the IR groups.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave lower cell-death markers than the other IR groups.

    Outcome
    DecreaseApoptotic markers (mitochondrial Bax, cleaved caspase-3, PARP)
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    Other IR groups (untreated, Mito alone, SS31 alone)
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    apoptotic markers (mitochondrial-Bax, cleaved-caspase-3, PARP)
    3 context sentences
    Summary · context
    all showed a pattern opposite that of LVEF.
    Summary · context
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  7. 13AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism

    In rats with myocardial ischemia-reperfusion injury, fibrosis markers showed a pattern opposite to ejection fraction, so they were lowest with SS31-Mito among the IR groups.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave lower scarring markers than the other IR groups.

    Outcome
    DecreaseFibrosis markers (p-Smad3, TGF-β)
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    Other IR groups (untreated, Mito alone, SS31 alone)
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    fibrosis markers (p-Smad3, TGF-β)
    3 context sentences
    Summary · context
    all showed a pattern opposite that of LVEF.
    Summary · context
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  8. 14AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism

    In rats with myocardial ischemia-reperfusion injury, the DNA-damage marker showed a pattern opposite to ejection fraction, so it was lowest with SS31-Mito among the IR groups.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave a lower DNA-damage marker than the other IR groups.

    Outcome
    DecreaseDNA damage (γ-H2AX)
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    Other IR groups (untreated, Mito alone, SS31 alone)
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    DNA-damage (γ-H2AX)
    3 context sentences
    Summary · context
    all showed a pattern opposite that of LVEF.
    Summary · context
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  9. 15AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism

    In rats with myocardial ischemia-reperfusion injury, sarcomere length showed a pattern opposite to ejection fraction, so it was lowest with SS31-Mito among the IR groups.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave shorter sarcomere length than the other IR groups.

    Outcome
    DecreaseSarcomere length
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    Other IR groups (untreated, Mito alone, SS31 alone)
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    sarcomere-length, and pressure/volume overload markers (BNP, β-MHC) all showed a pattern opposite that of LVEF.
    3 context sentences
    Summary · context
    all showed a pattern opposite that of LVEF.
    Summary · context
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  10. 16AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism

    In rats with myocardial ischemia-reperfusion injury, pressure and volume overload markers showed a pattern opposite to ejection fraction, so they were lowest with SS31-Mito among the IR groups.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave lower heart-strain markers than the other IR groups.

    Outcome
    DecreasePressure/volume overload markers (BNP, β-MHC)
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    Other IR groups (untreated, Mito alone, SS31 alone)
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    pressure/volume overload markers (BNP, β-MHC)
    3 context sentences
    Summary · context
    all showed a pattern opposite that of LVEF.
    Summary · context
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  11. 17AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism

    In rats with myocardial ischemia-reperfusion injury, anti-apoptotic markers followed the same pattern as ejection fraction, so they were highest with SS31-Mito among the IR groups.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave higher cell-protection markers than the other IR groups.

    Outcome
    IncreaseAnti-apoptotic markers (BMP-2, Smad1/5)
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    Other IR groups (untreated, Mito alone, SS31 alone)
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    Conversely, anti-apoptotic (BMP-2, Smad1/5) and energy integrity (PGC-1α/mitochondrial cytochrome-C) markers exhibited a pattern identical to that of LVEF.
    2 context sentences
    Summary · context
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  12. 18AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism

    In rats with myocardial ischemia-reperfusion injury, energy integrity markers followed the same pattern as ejection fraction, so they were highest with SS31-Mito among the IR groups.

    In plain wordsIn rats with heart injury after blocked blood flow, SS31 plus mitochondria gave higher cell-energy markers than the other IR groups.

    Outcome
    IncreaseEnergy integrity markers (PGC-1α, mitochondrial cytochrome c)
    Study

    ratn: not reported in source

    Myocardial ischemia-reperfusion injury in male Sprague-Dawley rats
    Comparator
    Other IR groups (untreated, Mito alone, SS31 alone)
    Outcome group
    Mitochondrial function · Cardiovascular

    Source sentences

    Summary
    Conversely, anti-apoptotic (BMP-2, Smad1/5) and energy integrity (PGC-1α/mitochondrial cytochrome-C) markers exhibited a pattern identical to that of LVEF.
    2 context sentences
    Summary · context
    LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone.
    Summary · context
    Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria).

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

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

    9 Oct 2026, 18:17 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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