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Study · Animal study (in vivo) · mouse · 2016

14 results

The tri-peptide GHK-Cu complex ameliorates lipopolysaccharide-induced acute lung injury in mice.

Park JR, Lee H, Kim SI, Yang SR

Oncotarget1 Sept 2016Cited by 48 (Europe PMC)

PMID27517151 (opens in a new tab)PMCIDPMC5295439 (opens in a new tab)DOI10.18632/oncotarget.11168 (opens in a new tab)PepBankPUB-27517151
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Summary

The tripeptide-copper complex glycyl-l-histidyl-l-lysine-Cu (II) (GHK-Cu) is involved in wound healing and tissue remodeling. Although GHK-Cu exhibits anti-aging and tissue renewing properties, its roles in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) are still unknown. Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo. GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI. Moreover, GHK-Cu attenuated LPS-induced lung histological alterations, suppressed the infiltration of inflammatory cells into the lung parenchyma in LPS-induced ALI in mice. Taken together, these findings demonstrate that GHK-Cu possesses a protective effect in LPS-induced ALI by inhibiting excessive inflammatory responses; accordingly it may represent a novel therapeutic approach for ALI/ARDS.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study14

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In mice with LPS-induced acute lung injury, GHK‑Cu treatment reduced reactive oxygen species production.

    In plain wordsIn mice with lung injury, GHK‑Cu lowered production of reactive oxygen species.

    Peptide
    GHK-Cu
    Outcome
    DecreaseROS production
    Study

    mousen: not reported in source

    LPS-induced acute lung injury
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI.
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mice with LPS-induced acute lung injury, GHK‑Cu treatment increased superoxide dismutase activity.

    In plain wordsIn mice with lung injury, GHK‑Cu raised the activity of the antioxidant enzyme SOD.

    Peptide
    GHK-Cu
    Outcome
    IncreaseSOD activity
    Study

    mousen: not reported in source

    LPS-induced acute lung injury
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI.
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice with LPS-induced acute lung injury, GHK‑Cu treatment decreased TNF-α production.

    In plain wordsIn mice with lung injury, GHK‑Cu lowered the inflammatory signal TNF-α.

    Peptide
    GHK-Cu
    Outcome
    DecreaseTNF-α production
    Study

    mousen: not reported in source

    LPS-induced acute lung injury
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI.
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mice with LPS-induced acute lung injury, GHK‑Cu treatment decreased IL-6 production.

    In plain wordsIn mice with lung injury, GHK‑Cu lowered the inflammatory signal IL-6.

    Peptide
    GHK-Cu
    Outcome
    DecreaseIL-6 production
    Study

    mousen: not reported in source

    LPS-induced acute lung injury
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI.
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mice with LPS-induced acute lung injury, GHK‑Cu treatment suppressed NF-κB p65 signaling.

    In plain wordsIn mice with lung injury, GHK‑Cu switched down the NF-κB p65 inflammation pathway.

    Peptide
    GHK-Cu
    Outcome
    DecreaseNF-κB p65 signaling
    Study

    mousen: not reported in source

    LPS-induced acute lung injury
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI.
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In mice with LPS-induced acute lung injury, GHK‑Cu treatment suppressed p38 MAPK signaling.

    In plain wordsIn mice with lung injury, GHK‑Cu switched down the p38 MAPK inflammation pathway.

    Peptide
    GHK-Cu
    Outcome
    Decreasep38 MAPK signaling
    Study

    mousen: not reported in source

    LPS-induced acute lung injury
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI.
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  7. 07AnimalAnimal study (in vivo)Efficacy outcome

    In mice with LPS-induced acute lung injury, GHK‑Cu attenuated lung histological alterations.

    In plain wordsIn mice with lung injury, GHK‑Cu reduced tissue damage seen under the microscope.

    Peptide
    GHK-Cu
    Outcome
    DecreaseLung histological alterations
    Study

    mousen: not reported in source

    LPS-induced acute lung injury
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu attenuated LPS-induced lung histological alterations
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  8. 08AnimalAnimal study (in vivo)Efficacy outcome

    In mice with LPS-induced acute lung injury, GHK‑Cu suppressed infiltration of inflammatory cells into the lung parenchyma.

    In plain wordsIn mice with lung injury, GHK‑Cu reduced the number of inflammatory cells entering lung tissue.

    Peptide
    GHK-Cu
    Outcome
    DecreaseInflammatory cell infiltration in lung
    Study

    mousen: not reported in source

    LPS-induced acute lung injury
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    suppressed the infiltration of inflammatory cells into the lung parenchyma
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  9. 09LabIn vitro (cells)Mechanism

    In LPS-stimulated RAW 264.7 macrophages, GHK‑Cu treatment reduced reactive oxygen species production.

    In plain wordsIn cells, GHK‑Cu lowered production of reactive oxygen species after an inflammatory trigger.

    Peptide
    GHK-Cu
    Outcome
    DecreaseROS production
    Study

    n: not reported in source

    LPS-stimulated RAW 264.7 macrophages
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI.
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  10. 10LabIn vitro (cells)Mechanism

    In LPS-stimulated RAW 264.7 macrophages, GHK‑Cu treatment increased superoxide dismutase activity.

    In plain wordsIn cells, GHK‑Cu raised the activity of the antioxidant enzyme SOD after an inflammatory trigger.

    Peptide
    GHK-Cu
    Outcome
    IncreaseSOD activity
    Study

    n: not reported in source

    LPS-stimulated RAW 264.7 macrophages
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI.
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  11. 11LabIn vitro (cells)Efficacy outcome

    In LPS-stimulated RAW 264.7 macrophages, GHK‑Cu treatment decreased TNF-α production.

    In plain wordsIn cells, GHK‑Cu lowered the inflammatory signal TNF-α after an inflammatory trigger.

    Peptide
    GHK-Cu
    Outcome
    DecreaseTNF-α production
    Study

    n: not reported in source

    LPS-stimulated RAW 264.7 macrophages
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI.
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  12. 12LabIn vitro (cells)Efficacy outcome

    In LPS-stimulated RAW 264.7 macrophages, GHK‑Cu treatment decreased IL-6 production.

    In plain wordsIn cells, GHK‑Cu lowered the inflammatory signal IL-6 after an inflammatory trigger.

    Peptide
    GHK-Cu
    Outcome
    DecreaseIL-6 production
    Study

    n: not reported in source

    LPS-stimulated RAW 264.7 macrophages
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI.
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  13. 13LabIn vitro (cells)Mechanism

    In LPS-stimulated RAW 264.7 macrophages, GHK‑Cu treatment suppressed NF-κB p65 signaling.

    In plain wordsIn cells, GHK‑Cu switched down the NF-κB p65 inflammation pathway after an inflammatory trigger.

    Peptide
    GHK-Cu
    Outcome
    DecreaseNF-κB p65 signaling
    Study

    n: not reported in source

    LPS-stimulated RAW 264.7 macrophages
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI.
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.
  14. 14LabIn vitro (cells)Mechanism

    In LPS-stimulated RAW 264.7 macrophages, GHK‑Cu treatment suppressed p38 MAPK signaling.

    In plain wordsIn cells, GHK‑Cu switched down the p38 MAPK inflammation pathway after an inflammatory trigger.

    Peptide
    GHK-Cu
    Outcome
    Decreasep38 MAPK signaling
    Study

    n: not reported in source

    LPS-stimulated RAW 264.7 macrophages
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI.
    1 context sentence
    Summary · context
    Therefore, we examined the effects of GHK-Cu in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in vitro and ALI in mice in vivo.

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 3Current

    9 Oct 2026, 18:17 UTC

    Study results updated

  2. Version 2

    9 Oct 2026, 03:03 UTC

    Study data updated · source update from Europe PMC

  3. Version 1

    9 Oct 2026, 02:56 UTC

    First added · source update from Europe PMC

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