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Study · Animal study (in vivo) · mouse · 2023

11 results

SS-31 Improves Cognitive Function in Sepsis-Associated Encephalopathy by Inhibiting the Drp1-NLRP3 Inflammasome Activation.

Zhong L, Ren X, Ai Y, Liu Z

Neuromolecular medicine4 Nov 2022Cited by 19 (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 study11

11 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 sepsis-associated encephalopathy, SS‑31 improved cognitive performance.

    In plain wordsIn mice with sepsis-related brain injury, SS‑31 improved thinking and memory performance.

    Outcome
    IncreaseCognitive performance
    Study

    mousen: not reported in source

    Cecal ligation and puncture sepsis-associated encephalopathy
    Outcome group
    Cognition and memory · Nervous system and cognition
    Studied dose
    Dose not stated · intraperitoneal · 7 daysAs given in this study (mouse).

    Source sentences

    Summary
    SS-31 improved cognitive performance and survival rate of mice and alleviated hippocampal inflammation, reactive oxygen species production, and excessive mitochondrial fission.
    1 context sentence
    Summary · context
    In mice, SS-31 was intraperitoneally administered for seven consecutive days after cecal ligation and puncture surgery.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with sepsis-associated encephalopathy, SS‑31 improved the survival rate.

    In plain wordsIn mice with sepsis-related brain injury, SS‑31 improved survival.

    Outcome
    IncreaseSurvival rate
    Study

    mousen: not reported in source

    Cecal ligation and puncture sepsis-associated encephalopathy
    Outcome group
    Mortality · Nervous system and cognition
    Studied dose
    Dose not stated · intraperitoneal · 7 daysAs given in this study (mouse).

    Source sentences

    Summary
    SS-31 improved cognitive performance and survival rate of mice and alleviated hippocampal inflammation, reactive oxygen species production, and excessive mitochondrial fission.
    1 context sentence
    Summary · context
    In mice, SS-31 was intraperitoneally administered for seven consecutive days after cecal ligation and puncture surgery.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mice with sepsis-associated encephalopathy, SS‑31 alleviated hippocampal inflammation.

    In plain wordsIn mice with sepsis-related brain injury, SS‑31 reduced inflammation in the hippocampus.

    Outcome
    DecreaseHippocampal inflammation
    Study

    mousen: not reported in source

    Cecal ligation and puncture sepsis-associated encephalopathy
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated · intraperitoneal · 7 daysAs given in this study (mouse).

    Source sentences

    Summary
    SS-31 improved cognitive performance and survival rate of mice and alleviated hippocampal inflammation, reactive oxygen species production, and excessive mitochondrial fission.
    1 context sentence
    Summary · context
    In mice, SS-31 was intraperitoneally administered for seven consecutive days after cecal ligation and puncture surgery.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In mice with sepsis-associated encephalopathy, SS‑31 alleviated reactive oxygen species production.

    In plain wordsIn mice with sepsis-related brain injury, SS‑31 lowered reactive oxygen species.

    Outcome
    DecreaseReactive oxygen species production
    Study

    mousen: not reported in source

    Cecal ligation and puncture sepsis-associated encephalopathy
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated · intraperitoneal · 7 daysAs given in this study (mouse).

    Source sentences

    Summary
    SS-31 improved cognitive performance and survival rate of mice and alleviated hippocampal inflammation, reactive oxygen species production, and excessive mitochondrial fission.
    1 context sentence
    Summary · context
    In mice, SS-31 was intraperitoneally administered for seven consecutive days after cecal ligation and puncture surgery.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mice with sepsis-associated encephalopathy, SS‑31 alleviated excessive mitochondrial fission.

    In plain wordsIn mice with sepsis-related brain injury, SS‑31 reduced excessive splitting of mitochondria.

    Outcome
    DecreaseExcessive mitochondrial fission
    Study

    mousen: not reported in source

    Cecal ligation and puncture sepsis-associated encephalopathy
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated · intraperitoneal · 7 daysAs given in this study (mouse).

    Source sentences

    Summary
    SS-31 improved cognitive performance and survival rate of mice and alleviated hippocampal inflammation, reactive oxygen species production, and excessive mitochondrial fission.
    1 context sentence
    Summary · context
    In mice, SS-31 was intraperitoneally administered for seven consecutive days after cecal ligation and puncture surgery.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In mice with sepsis-associated encephalopathy, SS‑31 attenuated the increase of NLRP3 in microglia.

    In plain wordsIn mice with sepsis-related brain injury, SS‑31 reduced a rise in the inflammation protein NLRP3 in microglia.

    Outcome
    DecreaseMicroglial NLRP3 increase
    Study

    mousen: not reported in source

    Cecal ligation and puncture sepsis-associated encephalopathy
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated · intraperitoneal · 7 daysAs given in this study (mouse).

    Source sentences

    Summary
    The increase of nucleotide-binding oligomerization domain 3 (NLRP3) and phosphorylated dynamin-related protein 1 (Drp1) ser616 in microglia was attenuated by SS-31.
    1 context sentence
    Summary · context
    In mice, SS-31 was intraperitoneally administered for seven consecutive days after cecal ligation and puncture surgery.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In mice with sepsis-associated encephalopathy, SS‑31 attenuated the increase of phosphorylated Drp1 Ser616 in microglia.

    In plain wordsIn mice with sepsis-related brain injury, SS‑31 reduced a rise in activated Drp1 in microglia.

    Outcome
    DecreaseMicroglial phosphorylated Drp1 Ser616 increase
    Study

    mousen: not reported in source

    Cecal ligation and puncture sepsis-associated encephalopathy
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated · intraperitoneal · 7 daysAs given in this study (mouse).

    Source sentences

    Summary
    The increase of nucleotide-binding oligomerization domain 3 (NLRP3) and phosphorylated dynamin-related protein 1 (Drp1) ser616 in microglia was attenuated by SS-31.
    1 context sentence
    Summary · context
    In mice, SS-31 was intraperitoneally administered for seven consecutive days after cecal ligation and puncture surgery.
  8. 08LabIn vitro (cells)Mechanism

    In BV-2 microglial cells, SS‑31 decreased activation of the NLRP3 inflammasome.

    In plain wordsIn microglial cells, SS‑31 reduced activation of the NLRP3 inflammasome.

    Outcome
    DecreaseNLRP3 inflammasome activation in BV-2 cells
    Study

    n: not reported in source

    BV-2 microglial cells with LPS/ATP induction
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 effectively decreased the activation of NLRP3 inflammasome, mitochondrial translocation of Drp1, excessive mitochondrial fission, and mitochondrial membrane recruitment of gasdermin-D N-terminal (GSDMD-N).
    1 context sentence
    Summary · context
    In vitro, the microglial cell line BV-2 was pre-treated with SS-31, followed by lipopolysaccharide/adenosine triphosphate induction.
  9. 09LabIn vitro (cells)Mechanism

    In BV-2 microglial cells, SS‑31 decreased mitochondrial translocation of Drp1.

    In plain wordsIn microglial cells, SS‑31 reduced movement of Drp1 to the mitochondria.

    Outcome
    DecreaseMitochondrial translocation of Drp1
    Study

    n: not reported in source

    BV-2 microglial cells with LPS/ATP induction
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 effectively decreased the activation of NLRP3 inflammasome, mitochondrial translocation of Drp1, excessive mitochondrial fission, and mitochondrial membrane recruitment of gasdermin-D N-terminal (GSDMD-N).
    1 context sentence
    Summary · context
    In vitro, the microglial cell line BV-2 was pre-treated with SS-31, followed by lipopolysaccharide/adenosine triphosphate induction.
  10. 10LabIn vitro (cells)Mechanism

    In BV-2 microglial cells, SS‑31 decreased excessive mitochondrial fission.

    In plain wordsIn microglial cells, SS‑31 reduced excessive splitting of mitochondria.

    Outcome
    DecreaseExcessive mitochondrial fission in BV-2 cells
    Study

    n: not reported in source

    BV-2 microglial cells with LPS/ATP induction
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 effectively decreased the activation of NLRP3 inflammasome, mitochondrial translocation of Drp1, excessive mitochondrial fission, and mitochondrial membrane recruitment of gasdermin-D N-terminal (GSDMD-N).
    1 context sentence
    Summary · context
    In vitro, the microglial cell line BV-2 was pre-treated with SS-31, followed by lipopolysaccharide/adenosine triphosphate induction.
  11. 11LabIn vitro (cells)Mechanism

    In BV-2 microglial cells, SS‑31 decreased mitochondrial membrane recruitment of gasdermin-D N-terminal.

    In plain wordsIn microglial cells, SS‑31 reduced the attachment of a cell-death protein fragment to mitochondria.

    Outcome
    DecreaseMitochondrial membrane recruitment of GSDMD-N
    Study

    n: not reported in source

    BV-2 microglial cells with LPS/ATP induction
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 effectively decreased the activation of NLRP3 inflammasome, mitochondrial translocation of Drp1, excessive mitochondrial fission, and mitochondrial membrane recruitment of gasdermin-D N-terminal (GSDMD-N).
    1 context sentence
    Summary · context
    In vitro, the microglial cell line BV-2 was pre-treated with SS-31, followed by lipopolysaccharide/adenosine triphosphate induction.

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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