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Study · In vitro (cells) · mouse · 2020

5 results

The Mitochondrial-Targeted Peptide, SS31, Protects Murine 661W Cells from Oxidative Damage via Induction of Autophagy.

He Y, He B, Zhang R, Quan Z, Xu Y, Chen Z, Ren Y

Journal of biomedical nanotechnology1 May 2020Cited by 1 (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

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In 661W cells, pre-treatment with 100 nM SS31 significantly attenuated hydrogen peroxide-mediated cytotoxicity.

    In plain wordsIn lab-grown eye cells, SS31 pre-treatment reduced the cell damage caused by hydrogen peroxide.

    Outcome
    DecreaseH2O2-mediated cytotoxicity
    Study

    mousen: not reported in source

    murine 661W cone photoreceptor cells with H2O2 oxidative injury
    Comparator
    H2O2 without SS31
    Outcome group
    Neuroprotection · Eye
    Studied dose
    100 nMAs given in this study (mouse).

    Measurements

    SS31 concentration
    100 nM
    661W cells

    Source sentences

    Summary
    Pre-treatment with 100 nM SS31 resulted in significant attenuation of H₂O₂-mediated cytotoxicity
    1 context sentence
    Summary · context
    To do so, we examined the viability of 661W cells in the presence of increasing concentrations of H₂O₂ with or without SS31 pre-treatment using the MTT assay and by expression of autophagy and apoptosis-associated proteins LC3-II/I, P62, and caspase-3.
  2. 02LabIn vitro (cells)Mechanism

    In 661W cells under oxidative stress, SS31 pre-treatment reduced ROS production.

    In plain wordsIn lab-grown eye cells, SS31 pre-treatment lowered reactive oxygen species under oxidative stress.

    Outcome
    DecreaseROS production
    Study

    mousen: not reported in source

    murine 661W cone photoreceptor cells with H2O2 oxidative injury
    Comparator
    H2O2 without SS31
    Outcome group
    Mitochondrial function · Eye
    Studied dose
    100 nMAs given in this study (mouse).

    Source sentences

    Summary
    Pre-treatment with 100 nM SS31 resulted in significant attenuation of H₂O₂-mediated cytotoxicity, together with reduced ROS production and enhanced autophagy observed in response to oxidative stress.
    1 context sentence
    Summary · context
    To do so, we examined the viability of 661W cells in the presence of increasing concentrations of H₂O₂ with or without SS31 pre-treatment using the MTT assay and by expression of autophagy and apoptosis-associated proteins LC3-II/I, P62, and caspase-3.
  3. 03LabIn vitro (cells)Mechanism

    In 661W cells under oxidative stress, SS31 pre-treatment enhanced autophagy.

    In plain wordsIn lab-grown eye cells, SS31 pre-treatment increased autophagy, the cell's recycling process, under oxidative stress.

    Outcome
    IncreaseAutophagy
    Study

    mousen: not reported in source

    murine 661W cone photoreceptor cells with H2O2 oxidative injury
    Comparator
    H2O2 without SS31
    Outcome group
    Neuroprotection · Eye
    Studied dose
    100 nMAs given in this study (mouse).

    Source sentences

    Summary
    Pre-treatment with 100 nM SS31 resulted in significant attenuation of H₂O₂-mediated cytotoxicity, together with reduced ROS production and enhanced autophagy observed in response to oxidative stress.
    1 context sentence
    Summary · context
    To do so, we examined the viability of 661W cells in the presence of increasing concentrations of H₂O₂ with or without SS31 pre-treatment using the MTT assay and by expression of autophagy and apoptosis-associated proteins LC3-II/I, P62, and caspase-3.
  4. 04LabIn vitro (cells)Mechanism

    In hydrogen peroxide-exposed 661W cells, SS31 caused significant changes in gene expression that suggested autophagy induction through mTORC1-mediated signaling.

    In plain wordsIn lab-grown eye cells, SS31 changed many genes, pointing to autophagy switched on through the mTORC1 pathway.

    Outcome
    MixedGene expression changes by mRNA-seq
    Study

    mousen: not reported in source

    murine 661W cone photoreceptor cells with H2O2 oxidative injury
    Outcome group
    Neuroprotection · Eye
    Studied dose
    100 nMAs given in this study (mouse).

    Source sentences

    Summary
    Furthermore, mRNAseq analysis revealed that SS31 promoted significant alterations in gene expression in 661W cells and suggested that autophagy was induced via the mTORC1-mediated signaling.
    1 context sentence
    Summary · context
    To do so, we examined the viability of 661W cells in the presence of increasing concentrations of H₂O₂ with or without SS31 pre-treatment using the MTT assay and by expression of autophagy and apoptosis-associated proteins LC3-II/I, P62, and caspase-3.

Studies that did not test the peptide alone1

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. 05LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism

    In 661W cells, the autophagy inhibitor bafA1 counteracted autophagy induced by SS31.

    In plain wordsIn lab-grown eye cells, a drug that blocks autophagy cancelled the autophagy caused by SS31.

    Outcome
    DecreaseAutophagy induced by SS31 with bafilomycin A1
    Study

    mousen: not reported in source

    murine 661W cone photoreceptor cells with H2O2 oxidative injury
    Comparator
    SS31 alone
    Outcome group
    Neuroprotection · Eye

    Source sentences

    Summary
    By contrast, administration of bafA1 counteracted autophagy induced by SS31.
    1 context sentence
    Summary · context
    To do so, we examined the viability of 661W cells in the presence of increasing concentrations of H₂O₂ with or without SS31 pre-treatment using the MTT assay and by expression of autophagy and apoptosis-associated proteins LC3-II/I, P62, and caspase-3.

    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

    10 Oct 2026, 08:19 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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