Skip to content

Study · Animal study (in vivo) · mouse · 2024

10 results

Mitochondria-targeted reactive oxygen species blockor SS-31 blocks hepatic stellate cell activation and alleviates hepatic fibrosis by regulating NLRP3 inflammasomes.

Liu L, Wei Y, Xie N, Cai H, Lin Y

Cellular and molecular biology (Noisy-le-Grand, France)29 Feb 2024Cited by 9 (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: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study10

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice with CCl4-induced liver fibrosis, SS‑31 treatment significantly reduced liver inflammation.

    In plain wordsIn mice with liver scarring, SS‑31 clearly reduced liver inflammation.

    Outcome
    DecreaseLiver inflammation
    Study

    mousen: not reported in source

    CCl4-induced liver fibrosis
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    After SS-31 treatment, liver inflammation and collagen deposition were significantly reduced.
    1 context sentence
    Summary · context
    Liver fibrosis was induced in mice using CCl4, and subsequently, histopathological changes were observed through HE staining and Masson staining.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with CCl4-induced liver fibrosis, SS‑31 treatment significantly reduced collagen deposition in the liver.

    In plain wordsIn mice with liver scarring, SS‑31 clearly reduced collagen build-up in the liver.

    Outcome
    DecreaseLiver collagen deposition
    Study

    mousen: not reported in source

    CCl4-induced liver fibrosis
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    After SS-31 treatment, liver inflammation and collagen deposition were significantly reduced.
    1 context sentence
    Summary · context
    Liver fibrosis was induced in mice using CCl4, and subsequently, histopathological changes were observed through HE staining and Masson staining.
  3. 03LabIn vitro (cells)Mechanism

    In TGF-beta1-activated hepatic stellate cells, SS‑31 treatment decreased mitochondrial ROS expression.

    In plain wordsIn lab-grown liver cells, SS‑31 lowered the level of harmful reactive oxygen molecules in mitochondria.

    Outcome
    DecreaseMitochondrial ROS expression
    Study

    n: not reported in source

    TGF-beta1-activated hepatic stellate cells
    Outcome group
    Mitochondrial function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    After SS-31 treatment, mitochondrial ROS expression decreased, MMP recovered, ATP level increased, HSC proliferation decreased, apoptosis increased, and the expressions of COL1A1, α-SMA, and NLRP3 inflammasome decreased.
    1 context sentence
    Summary · context
    TGF-β1 was employed to induce HSC activation, while MitoSOX Red was utilized to assess the presence of mitochondrial ROS.
  4. 04LabIn vitro (cells)Mechanism

    In TGF-beta1-activated hepatic stellate cells, SS‑31 treatment recovered the mitochondrial membrane potential.

    In plain wordsIn lab-grown liver cells, SS‑31 restored the electrical charge across the mitochondrial membrane.

    Outcome
    IncreaseMitochondrial membrane potential
    Study

    n: not reported in source

    TGF-beta1-activated hepatic stellate cells
    Outcome group
    Mitochondrial function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    After SS-31 treatment, mitochondrial ROS expression decreased, MMP recovered, ATP level increased, HSC proliferation decreased, apoptosis increased, and the expressions of COL1A1, α-SMA, and NLRP3 inflammasome decreased.
    1 context sentence
    Summary · context
    TGF-β1 was employed to induce HSC activation, while MitoSOX Red was utilized to assess the presence of mitochondrial ROS.
  5. 05LabIn vitro (cells)Mechanism

    In TGF-beta1-activated hepatic stellate cells, SS‑31 treatment increased ATP level.

    In plain wordsIn lab-grown liver cells, SS‑31 raised the energy molecule ATP.

    Outcome
    IncreaseATP level
    Study

    n: not reported in source

    TGF-beta1-activated hepatic stellate cells
    Outcome group
    Mitochondrial function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    After SS-31 treatment, mitochondrial ROS expression decreased, MMP recovered, ATP level increased, HSC proliferation decreased, apoptosis increased, and the expressions of COL1A1, α-SMA, and NLRP3 inflammasome decreased.
    1 context sentence
    Summary · context
    TGF-β1 was employed to induce HSC activation, while MitoSOX Red was utilized to assess the presence of mitochondrial ROS.
  6. 06LabIn vitro (cells)Mechanism

    In TGF-beta1-activated hepatic stellate cells, SS‑31 treatment decreased cell proliferation.

    In plain wordsIn lab-grown liver cells, SS‑31 slowed cell growth.

    Outcome
    DecreaseHepatic stellate cell proliferation
    Study

    n: not reported in source

    TGF-beta1-activated hepatic stellate cells
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    After SS-31 treatment, mitochondrial ROS expression decreased, MMP recovered, ATP level increased, HSC proliferation decreased, apoptosis increased, and the expressions of COL1A1, α-SMA, and NLRP3 inflammasome decreased.
    1 context sentence
    Summary · context
    TGF-β1 was employed to induce HSC activation, while MitoSOX Red was utilized to assess the presence of mitochondrial ROS.
  7. 07LabIn vitro (cells)Mechanism

    In TGF-beta1-activated hepatic stellate cells, SS‑31 treatment increased apoptosis.

    In plain wordsIn lab-grown liver cells, SS‑31 increased programmed cell death.

    Outcome
    IncreaseHepatic stellate cell apoptosis
    Study

    n: not reported in source

    TGF-beta1-activated hepatic stellate cells
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    After SS-31 treatment, mitochondrial ROS expression decreased, MMP recovered, ATP level increased, HSC proliferation decreased, apoptosis increased, and the expressions of COL1A1, α-SMA, and NLRP3 inflammasome decreased.
    1 context sentence
    Summary · context
    TGF-β1 was employed to induce HSC activation, while MitoSOX Red was utilized to assess the presence of mitochondrial ROS.
  8. 08LabIn vitro (cells)Mechanism

    In TGF-beta1-activated hepatic stellate cells, SS‑31 treatment decreased the expression of the fibrosis marker COL1A1.

    In plain wordsIn lab-grown liver cells, SS‑31 lowered the scarring marker COL1A1.

    Outcome
    DecreaseCOL1A1 expression
    Study

    n: not reported in source

    TGF-beta1-activated hepatic stellate cells
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    After SS-31 treatment, mitochondrial ROS expression decreased, MMP recovered, ATP level increased, HSC proliferation decreased, apoptosis increased, and the expressions of COL1A1, α-SMA, and NLRP3 inflammasome decreased.
    1 context sentence
    Summary · context
    TGF-β1 was employed to induce HSC activation, while MitoSOX Red was utilized to assess the presence of mitochondrial ROS.
  9. 09LabIn vitro (cells)Mechanism

    In TGF-beta1-activated hepatic stellate cells, SS‑31 treatment decreased the expression of the fibrosis marker alpha-SMA.

    In plain wordsIn lab-grown liver cells, SS‑31 lowered the scarring marker alpha-SMA.

    Outcome
    Decreasealpha-SMA expression
    Study

    n: not reported in source

    TGF-beta1-activated hepatic stellate cells
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    After SS-31 treatment, mitochondrial ROS expression decreased, MMP recovered, ATP level increased, HSC proliferation decreased, apoptosis increased, and the expressions of COL1A1, α-SMA, and NLRP3 inflammasome decreased.
    1 context sentence
    Summary · context
    TGF-β1 was employed to induce HSC activation, while MitoSOX Red was utilized to assess the presence of mitochondrial ROS.
  10. 10LabIn vitro (cells)Mechanism

    In TGF-beta1-activated hepatic stellate cells, SS‑31 treatment decreased the expression of the NLRP3 inflammasome.

    In plain wordsIn lab-grown liver cells, SS‑31 lowered the level of the NLRP3 inflammasome, an inflammation complex.

    Outcome
    DecreaseNLRP3 inflammasome expression
    Study

    n: not reported in source

    TGF-beta1-activated hepatic stellate cells
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    After SS-31 treatment, mitochondrial ROS expression decreased, MMP recovered, ATP level increased, HSC proliferation decreased, apoptosis increased, and the expressions of COL1A1, α-SMA, and NLRP3 inflammasome decreased.
    1 context sentence
    Summary · context
    TGF-β1 was employed to induce HSC activation, while MitoSOX Red was utilized to assess the presence of mitochondrial ROS.

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.

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