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Study · Animal study (in vivo) · mouse · 2021

23 results

Mitochondrial-Targeting Antioxidant SS-31 Suppresses Airway Inflammation and Oxidative Stress Induced by Cigarette Smoke.

Yang DQ, Zuo QN, Wang T, Xu D, Lian L, Gao LJ, Wan C, Chen L, Wen FQ, Shen YC

Oxidative medicine and cellular longevity15 Jun 2021Cited by 26 (Europe PMC)

PMID34221235 (opens in a new tab)PMCIDPMC8219423 (opens in a new tab)DOI10.1155/2021/6644238 (opens in a new tab)PepBankPUB-34221235
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Summary

This study investigated whether the mitochondrial-targeted peptide SS-31 can protect against cigarette smoke- (CS-) induced airway inflammation and oxidative stress in vitro and in vivo. Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure. Pathologic changes and oxidative stress in lung tissue, inflammatory cell counts, and proinflammatory cytokine levels in bronchoalveolar lavage fluid (BALF) were examined. The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues. SS-31 attenuated CS-induced inflammatory injury of the airway and reduced total cell, neutrophil, and macrophage counts and tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, and matrix metalloproteinase (MMP) 9 levels in BALF. SS-31 also attenuated CS-induced oxidative stress by decreasing malondialdehyde (MDA) and myeloperoxidase (MPO) activities and increasing that of superoxide dismutase (SOD). It also reversed CS-induced changes in the expression of mitochondrial fission protein (MFF) and optic atrophy (OPA) 1 and reduced the amount of cytochrome c released into the cytosol. Pretreatment with SS-31 normalized TNF-α, IL-6, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE-treated BEAS-2B cells and reversed the changes in MFF and OPA1 expression. RNA sequencing and western blot analysis showed that SS-31 inhibited CS-induced activation of the mitogen-activated protein kinase (MAPK) signaling pathway in vitro and in vivo. Thus, SS-31 alleviates CS-induced airway inflammation and oxidative stress via modulation of mitochondrial function and regulation of MAPK signaling and thus has therapeutic potential for the treatment of airway disorders caused by smoking.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study23

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to cigarette smoke, SS‑31 attenuated inflammatory injury of the airway.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 reduced inflammatory damage in the airway.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseCS-induced inflammatory injury of the airway
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 attenuated CS-induced inflammatory injury of the airway and reduced total cell, neutrophil, and macrophage counts and tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, and matrix metalloproteinase (MMP) 9 levels in BALF.
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to cigarette smoke, SS‑31 reduced total cell counts in bronchoalveolar lavage fluid.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 lowered the number of cells in lung fluid.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseTotal cell count in BALF
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 attenuated CS-induced inflammatory injury of the airway and reduced total cell, neutrophil, and macrophage counts and tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, and matrix metalloproteinase (MMP) 9 levels in BALF.
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to cigarette smoke, SS‑31 reduced neutrophil counts in bronchoalveolar lavage fluid.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 lowered neutrophil numbers in lung fluid.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseNeutrophil count in BALF
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 attenuated CS-induced inflammatory injury of the airway and reduced total cell, neutrophil, and macrophage counts and tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, and matrix metalloproteinase (MMP) 9 levels in BALF.
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to cigarette smoke, SS‑31 reduced macrophage counts in bronchoalveolar lavage fluid.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 lowered macrophage numbers in lung fluid.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMacrophage count in BALF
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 attenuated CS-induced inflammatory injury of the airway and reduced total cell, neutrophil, and macrophage counts and tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, and matrix metalloproteinase (MMP) 9 levels in BALF.
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mice exposed to cigarette smoke, SS‑31 reduced TNF-α levels in bronchoalveolar lavage fluid.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 lowered the inflammatory signal TNF-α in lung fluid.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseTNF-α level in BALF
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 attenuated CS-induced inflammatory injury of the airway and reduced total cell, neutrophil, and macrophage counts and tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, and matrix metalloproteinase (MMP) 9 levels in BALF.
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In mice exposed to cigarette smoke, SS‑31 reduced interleukin-6 levels in bronchoalveolar lavage fluid.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 lowered the inflammatory signal IL-6 in lung fluid.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseIL-6 level in BALF
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 attenuated CS-induced inflammatory injury of the airway and reduced total cell, neutrophil, and macrophage counts and tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, and matrix metalloproteinase (MMP) 9 levels in BALF.
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In mice exposed to cigarette smoke, SS‑31 reduced MMP9 levels in bronchoalveolar lavage fluid.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 lowered MMP9, a tissue-damaging enzyme, in lung fluid.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMMP9 level in BALF
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 attenuated CS-induced inflammatory injury of the airway and reduced total cell, neutrophil, and macrophage counts and tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, and matrix metalloproteinase (MMP) 9 levels in BALF.
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In mice exposed to cigarette smoke, SS‑31 decreased malondialdehyde activity as a marker of oxidative stress.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 lowered a marker of oxidative damage (MDA).

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMDA activity in lung
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 also attenuated CS-induced oxidative stress by decreasing malondialdehyde (MDA) and myeloperoxidase (MPO) activities and increasing that of superoxide dismutase (SOD).
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In mice exposed to cigarette smoke, SS‑31 decreased myeloperoxidase activity.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 lowered the activity of the inflammation enzyme MPO.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMPO activity in lung
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 also attenuated CS-induced oxidative stress by decreasing malondialdehyde (MDA) and myeloperoxidase (MPO) activities and increasing that of superoxide dismutase (SOD).
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  10. 10AnimalAnimal study (in vivo)Mechanism

    In mice exposed to cigarette smoke, SS‑31 increased superoxide dismutase activity.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 raised the activity of the antioxidant enzyme SOD.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseSOD activity in lung
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 also attenuated CS-induced oxidative stress by decreasing malondialdehyde (MDA) and myeloperoxidase (MPO) activities and increasing that of superoxide dismutase (SOD).
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  11. 11AnimalAnimal study (in vivo)Mechanism

    In mice exposed to cigarette smoke, SS‑31 reversed the CS-induced change in expression of the mitochondrial fission protein MFF.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 reversed the smoke-induced change in a mitochondrial protein (MFF).

    Peptide
    Elamipretide (SS-31)
    Outcome
    Direction not reportedMFF expression
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    It also reversed CS-induced changes in the expression of mitochondrial fission protein (MFF) and optic atrophy (OPA) 1 and reduced the amount of cytochrome c released into the cytosol.
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  12. 12AnimalAnimal study (in vivo)Mechanism

    In mice exposed to cigarette smoke, SS‑31 reversed the CS-induced change in expression of OPA1.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 reversed the smoke-induced change in a mitochondrial protein (OPA1).

    Peptide
    Elamipretide (SS-31)
    Outcome
    Direction not reportedOPA1 expression
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    It also reversed CS-induced changes in the expression of mitochondrial fission protein (MFF) and optic atrophy (OPA) 1 and reduced the amount of cytochrome c released into the cytosol.
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  13. 13AnimalAnimal study (in vivo)Mechanism

    In mice exposed to cigarette smoke, SS‑31 reduced the amount of cytochrome c released into the cytosol.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 reduced the release of cytochrome c from mitochondria.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseCytochrome c release into the cytosol
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    It also reversed CS-induced changes in the expression of mitochondrial fission protein (MFF) and optic atrophy (OPA) 1 and reduced the amount of cytochrome c released into the cytosol.
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  14. 14AnimalAnimal study (in vivo)Mechanism

    In mice exposed to cigarette smoke, SS‑31 inhibited CS-induced activation of the MAPK signaling pathway.

    In plain wordsIn mice exposed to cigarette smoke, SS‑31 blocked smoke-induced activation of the MAPK signalling pathway.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMAPK pathway activation in vivo
    Study

    mousen: not reported in source

    Cigarette smoke-induced airway inflammation
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    RNA sequencing and western blot analysis showed that SS-31 inhibited CS-induced activation of the mitogen-activated protein kinase (MAPK) signaling pathway in vitro and in vivo.
    1 context sentence
    Summary · context
    Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, and those in the experimental group were pretreated with SS-31 1 h before CS exposure.
  15. 15LabIn vitro (cells)Mechanism

    In BEAS-2B cells treated with cigarette smoke extract, SS‑31 pretreatment normalized TNF-α expression.

    In plain wordsIn lab lung cells exposed to smoke extract, SS‑31 pretreatment brought the inflammatory signal TNF-α back to normal.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseTNF-α expression in CSE-treated cells
    Study

    n: not reported in source

    BEAS-2B cells treated with cigarette smoke extract
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with SS-31 normalized TNF-α, IL-6, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE-treated BEAS-2B cells and reversed the changes in MFF and OPA1 expression.
    1 context sentence
    Summary · context
    The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues.
  16. 16LabIn vitro (cells)Mechanism

    In BEAS-2B cells treated with cigarette smoke extract, SS‑31 pretreatment normalized IL-6 expression.

    In plain wordsIn lab lung cells exposed to smoke extract, SS‑31 pretreatment brought the inflammatory signal IL-6 back to normal.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseIL-6 expression in CSE-treated cells
    Study

    n: not reported in source

    BEAS-2B cells treated with cigarette smoke extract
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with SS-31 normalized TNF-α, IL-6, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE-treated BEAS-2B cells and reversed the changes in MFF and OPA1 expression.
    1 context sentence
    Summary · context
    The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues.
  17. 17LabIn vitro (cells)Mechanism

    In BEAS-2B cells treated with cigarette smoke extract, SS‑31 pretreatment normalized MMP9 expression.

    In plain wordsIn lab lung cells exposed to smoke extract, SS‑31 pretreatment brought MMP9 back to normal.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMMP9 expression in CSE-treated cells
    Study

    n: not reported in source

    BEAS-2B cells treated with cigarette smoke extract
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with SS-31 normalized TNF-α, IL-6, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE-treated BEAS-2B cells and reversed the changes in MFF and OPA1 expression.
    1 context sentence
    Summary · context
    The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues.
  18. 18LabIn vitro (cells)Mechanism

    In BEAS-2B cells treated with cigarette smoke extract, SS‑31 pretreatment normalized malondialdehyde activity.

    In plain wordsIn lab lung cells exposed to smoke extract, SS‑31 pretreatment brought an oxidative damage marker (MDA) back to normal.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMDA activity in CSE-treated cells
    Study

    n: not reported in source

    BEAS-2B cells treated with cigarette smoke extract
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with SS-31 normalized TNF-α, IL-6, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE-treated BEAS-2B cells and reversed the changes in MFF and OPA1 expression.
    1 context sentence
    Summary · context
    The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues.
  19. 19LabIn vitro (cells)Mechanism

    In BEAS-2B cells treated with cigarette smoke extract, SS‑31 pretreatment normalized superoxide dismutase activity.

    In plain wordsIn lab lung cells exposed to smoke extract, SS‑31 pretreatment brought the antioxidant enzyme SOD back to normal.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseSOD activity in CSE-treated cells
    Study

    n: not reported in source

    BEAS-2B cells treated with cigarette smoke extract
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with SS-31 normalized TNF-α, IL-6, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE-treated BEAS-2B cells and reversed the changes in MFF and OPA1 expression.
    1 context sentence
    Summary · context
    The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues.
  20. 20LabIn vitro (cells)Mechanism

    In BEAS-2B cells treated with cigarette smoke extract, SS‑31 pretreatment normalized reactive oxygen species generation.

    In plain wordsIn lab lung cells exposed to smoke extract, SS‑31 pretreatment brought reactive oxygen species back to normal.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseROS generation in CSE-treated cells
    Study

    n: not reported in source

    BEAS-2B cells treated with cigarette smoke extract
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with SS-31 normalized TNF-α, IL-6, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE-treated BEAS-2B cells and reversed the changes in MFF and OPA1 expression.
    1 context sentence
    Summary · context
    The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues.
  21. 21LabIn vitro (cells)Mechanism

    In BEAS-2B cells treated with cigarette smoke extract, SS‑31 pretreatment reversed the changes in MFF expression.

    In plain wordsIn lab lung cells exposed to smoke extract, SS‑31 pretreatment reversed changes in a mitochondrial protein (MFF).

    Peptide
    Elamipretide (SS-31)
    Outcome
    Direction not reportedMFF expression in CSE-treated cells
    Study

    n: not reported in source

    BEAS-2B cells treated with cigarette smoke extract
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with SS-31 normalized TNF-α, IL-6, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE-treated BEAS-2B cells and reversed the changes in MFF and OPA1 expression.
    1 context sentence
    Summary · context
    The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues.
  22. 22LabIn vitro (cells)Mechanism

    In BEAS-2B cells treated with cigarette smoke extract, SS‑31 pretreatment reversed the changes in OPA1 expression.

    In plain wordsIn lab lung cells exposed to smoke extract, SS‑31 pretreatment reversed changes in a mitochondrial protein (OPA1).

    Peptide
    Elamipretide (SS-31)
    Outcome
    Direction not reportedOPA1 expression in CSE-treated cells
    Study

    n: not reported in source

    BEAS-2B cells treated with cigarette smoke extract
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with SS-31 normalized TNF-α, IL-6, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE-treated BEAS-2B cells and reversed the changes in MFF and OPA1 expression.
    1 context sentence
    Summary · context
    The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues.
  23. 23LabIn vitro (cells)Mechanism

    In cell experiments, SS‑31 inhibited cigarette smoke-induced activation of the MAPK signaling pathway.

    In plain wordsIn lab cells, SS‑31 blocked smoke-induced activation of the MAPK signalling pathway.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMAPK pathway activation in vitro
    Study

    n: not reported in source

    BEAS-2B cells treated with cigarette smoke extract
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    RNA sequencing and western blot analysis showed that SS-31 inhibited CS-induced activation of the mitogen-activated protein kinase (MAPK) signaling pathway in vitro and in vivo.
    1 context sentence
    Summary · context
    The mechanistic basis for the effects of SS-31 on CS extract- (CSE-) induced airway inflammation and oxidative stress was investigated using BEAS-2B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues.

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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