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Study · Animal study (in vivo) · mouse · 2025

20 results

Exploring the beneficial effects of GHK-Cu on an experimental model of colitis and the underlying mechanisms.

Mao S, Huang J, Li J, Sun F, Zhang Q, Cheng Q, Zeng W, Lei D, Wang S, Yao J

Frontiers in pharmacology2 Jul 2025Cited by 2 (Europe PMC)

PMID40672369 (opens in a new tab)PMCIDPMC12263609 (opens in a new tab)DOI10.3389/fphar.2025.1551843 (opens in a new tab)PepBankPUB-40672369
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Summary

IntroductionUlcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) characterized by mucosal damage and impaired epithelial barrier function. While glycyl-l-histidyl-l-lysine-copper (GHK-Cu) exhibits known anti-inflammatory properties, its therapeutic mechanisms in UC remain undefined. This study was designed to systematically evaluate the therapeutic potential of GHK-Cu in a dextran sulfate sodium (DSS)-induced murine model of UC, with particular emphasis on elucidating its regulatory effects on the NAD-dependent deacetylase sirtuin-1 (SIRT1)/signal transducer and activator of transcription 3 (STAT3) signaling pathway.MethodsUC was induced in BALB/c mice with 3% DSS for 14 days. The protein expression levels of tight junction associated protein-1 (ZO-1), Occludin, inflammatory factors interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α, SIRT1, STAT3, p-STAT3, and retinoic acid receptor-related orphan receptor gamma t (RORγt) were detected by Western blot. Histopathological changes were evaluated by Hematoxylin and Eosin (H&E) and Alcian blue-periodic acid-Schiff (AB-PAS). Network pharmacology and molecular docking were used to predict the core targets of GHK Cu in the treatment of UC. An in vitro UC model was also established in mouse peritoneal macrophages (MPMs) using lipopolysaccharide (LPS), and a co culture model was constructed using mouse colonic epithelial cells (MCECs) and MPMs to examine the role of GHK Cu in promoting mucosal healing. STAT3 was silenced by gene transfection technology to verify the core role of STAT3 in GHK Cu treatment of UC.ResultsGHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair. Additionally, a co-culture system of MCECs and MPMs revealed that GHK-Cu facilitated MCECs healing, impaired by DSS, by upregulating ZO-1 and Occludin expression. Subsequently, network pharmacology and molecular docking identified SIRT1 as a potential target of GHK-Cu. Results showed that GHK-Cu upregulated SIRT1 protein expression and suppressed the expression of phosphorylated p-STAT3 in colon tissue and MCECs of the co-culture model. Our findings revealed that after transfection with STAT3-targeting siRNA (siSTAT3), the stimulant effect of GHK-Cu on the healing of MCECs and the effect on the protein expression of ZO-1 and Occludin is canceled. Nevertheless, after transfection with siSTAT3, it could inhibit the expression of inflammatory factors in conjunction with GHK-Cu. Furthermore, we found that GHK-Cu could inhibit RORγt expression in the colon tissue of UC mice.DiscussionThis study found that GHK-Cu demonstrated significant therapeutic effects in DSS-induced UC in mice. GHK-Cu may promote mucosal healing and enhance tight junction protein expression by regulating the SIRT1/STAT3 pathway. In addition to suppressing p-STAT3 expression, GHK-Cu may utilize additional pathways to inhibit inflammatory factors. Furthermore, GHK-Cu may reduce the number of Th17 cells. In summary, GHK-Cu may treat UC by acting on the SIRT1/STAT3 pathway.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study20

18 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 DSS-induced colitis, GHK‑Cu alleviated weight loss.

    In plain wordsIn mice with induced colitis, GHK‑Cu lessened weight loss.

    Peptide
    GHK-Cu
    Outcome
    DecreaseWeight loss
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Body weight · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with DSS-induced colitis, GHK‑Cu improved the disease activity index.

    In plain wordsIn mice with induced colitis, GHK‑Cu improved the disease activity score.

    Peptide
    GHK-Cu
    Outcome
    DecreaseDisease activity index
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice with DSS-induced colitis, GHK‑Cu reduced colonic edema.

    In plain wordsIn mice with induced colitis, GHK‑Cu reduced swelling of the colon.

    Peptide
    GHK-Cu
    Outcome
    DecreaseColonic edema
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mice with DSS-induced colitis, GHK‑Cu reduced colon shortening.

    In plain wordsIn mice with induced colitis, GHK‑Cu reduced shortening of the colon.

    Peptide
    GHK-Cu
    Outcome
    DecreaseColon shortening
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In mice with DSS-induced colitis, GHK‑Cu attenuated inflammatory damage.

    In plain wordsIn mice with induced colitis, GHK‑Cu reduced inflammatory damage to the colon.

    Peptide
    GHK-Cu
    Outcome
    DecreaseInflammatory damage
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  6. 06AnimalAnimal study (in vivo)Efficacy outcome

    In mice with DSS-induced colitis, GHK‑Cu increased goblet cell numbers.

    In plain wordsIn mice with induced colitis, GHK‑Cu increased the number of mucus-making goblet cells.

    Peptide
    GHK-Cu
    Outcome
    IncreaseGoblet cell number
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  7. 07AnimalAnimal study (in vivo)Efficacy outcome

    In mice with DSS-induced colitis, GHK‑Cu suppressed the inflammatory cytokine TNF-α.

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

    Peptide
    GHK-Cu
    Outcome
    DecreaseTNF-α
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  8. 08AnimalAnimal study (in vivo)Efficacy outcome

    In mice with DSS-induced colitis, GHK‑Cu suppressed the inflammatory cytokine IL-6.

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

    Peptide
    GHK-Cu
    Outcome
    DecreaseIL-6
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  9. 09AnimalAnimal study (in vivo)Efficacy outcome

    In mice with DSS-induced colitis, GHK‑Cu suppressed the inflammatory cytokine IL-1β.

    In plain wordsIn mice with induced colitis, GHK‑Cu lowered the inflammatory signal IL-1β.

    Peptide
    GHK-Cu
    Outcome
    DecreaseIL-1β
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  10. 10AnimalAnimal study (in vivo)Efficacy outcome

    In mice with DSS-induced colitis, GHK‑Cu promoted mucosal repair.

    In plain wordsIn mice with induced colitis, GHK‑Cu helped the gut lining to repair.

    Peptide
    GHK-Cu
    Outcome
    IncreaseMucosal repair
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  11. 11AnimalAnimal study (in vivo)Mechanism

    In colon tissue of DSS-induced colitis mice and in the co-culture model, GHK‑Cu upregulated SIRT1 protein expression.

    In plain wordsIn mice with induced colitis and in mouse cells, GHK‑Cu raised levels of the protein SIRT1.

    Peptide
    GHK-Cu
    Outcome
    IncreaseSIRT1 protein expression
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Receptor activity and mechanism · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Results showed that GHK-Cu upregulated SIRT1 protein expression and suppressed the expression of phosphorylated p-STAT3 in colon tissue and MCECs of the co-culture model.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  12. 12AnimalAnimal study (in vivo)Mechanism

    In colon tissue of DSS-induced colitis mice and in the co-culture model, GHK‑Cu suppressed phosphorylated STAT3 expression.

    In plain wordsIn mice with induced colitis and in mouse cells, GHK‑Cu lowered levels of the active form of STAT3.

    Peptide
    GHK-Cu
    Outcome
    Decreasep-STAT3 expression
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Receptor activity and mechanism · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Results showed that GHK-Cu upregulated SIRT1 protein expression and suppressed the expression of phosphorylated p-STAT3 in colon tissue and MCECs of the co-culture model.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  13. 13AnimalAnimal study (in vivo)Mechanism

    In colon tissue of mice with DSS-induced colitis, GHK‑Cu inhibited RORγt expression.

    In plain wordsIn mice with induced colitis, GHK‑Cu lowered levels of RORγt in the colon.

    Peptide
    GHK-Cu
    Outcome
    DecreaseRORγt expression in colon tissue
    Study

    mousen: not reported in source

    DSS-induced ulcerative colitis model
    Outcome group
    Receptor activity and mechanism · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, we found that GHK-Cu could inhibit RORγt expression in the colon tissue of UC mice.
    1 context sentence
    Summary · context
    UC was induced in BALB/c mice with 3% DSS for 14 days.
  14. 14LabIn vitro (cells)Efficacy outcome

    In a co-culture of mouse colonic epithelial cells and macrophages, GHK‑Cu facilitated healing of epithelial cells impaired by DSS.

    In plain wordsIn mouse cells, GHK‑Cu helped gut lining cells heal after damage by DSS.

    Peptide
    GHK-Cu
    Outcome
    IncreaseColonic epithelial cell healing in co-culture
    Study

    mousen: not reported in source

    MCEC and MPM co-culture
    Outcome group
    Wound healing · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu facilitated MCECs healing, impaired by DSS, by upregulating ZO-1 and Occludin expression.
    1 context sentence
    Summary · context
    An in vitro UC model was also established in mouse peritoneal macrophages (MPMs) using lipopolysaccharide (LPS), and a co culture model was constructed using mouse colonic epithelial cells (MCECs) and MPMs to examine the role of GHK Cu in promoting mucosal healing.
  15. 15LabIn vitro (cells)Efficacy outcome

    In a co-culture of mouse colonic epithelial cells and macrophages, GHK‑Cu upregulated ZO-1 expression.

    In plain wordsIn mouse cells, GHK‑Cu raised levels of the tight junction protein ZO-1.

    Peptide
    GHK-Cu
    Outcome
    IncreaseZO-1 expression
    Study

    mousen: not reported in source

    MCEC and MPM co-culture
    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Additionally, a co-culture system of MCECs and MPMs revealed that GHK-Cu facilitated MCECs healing, impaired by DSS, by upregulating ZO-1 and Occludin expression.
    1 context sentence
    Summary · context
    An in vitro UC model was also established in mouse peritoneal macrophages (MPMs) using lipopolysaccharide (LPS), and a co culture model was constructed using mouse colonic epithelial cells (MCECs) and MPMs to examine the role of GHK Cu in promoting mucosal healing.
  16. 16LabIn vitro (cells)Efficacy outcome

    In a co-culture of mouse colonic epithelial cells and macrophages, GHK‑Cu upregulated Occludin expression.

    In plain wordsIn mouse cells, GHK‑Cu raised levels of the tight junction protein Occludin.

    Peptide
    GHK-Cu
    Outcome
    IncreaseOccludin expression
    Study

    mousen: not reported in source

    MCEC and MPM co-culture
    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Additionally, a co-culture system of MCECs and MPMs revealed that GHK-Cu facilitated MCECs healing, impaired by DSS, by upregulating ZO-1 and Occludin expression.
    1 context sentence
    Summary · context
    An in vitro UC model was also established in mouse peritoneal macrophages (MPMs) using lipopolysaccharide (LPS), and a co culture model was constructed using mouse colonic epithelial cells (MCECs) and MPMs to examine the role of GHK Cu in promoting mucosal healing.
  17. 17LabIn vitro (cells)Mechanism

    After STAT3 silencing with siRNA, the stimulant effect of GHK‑Cu on epithelial cell healing was canceled.

    In plain wordsIn mouse cells, silencing STAT3 removed the healing effect of GHK‑Cu.

    Peptide
    GHK-Cu
    Outcome
    No significant changeGHK-Cu effect on epithelial cell healing after STAT3 silencing
    Study

    mousen: not reported in source

    MCEC and MPM co-culture, siSTAT3
    Outcome group
    Receptor activity and mechanism · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Our findings revealed that after transfection with STAT3-targeting siRNA (siSTAT3), the stimulant effect of GHK-Cu on the healing of MCECs and the effect on the protein expression of ZO-1 and Occludin is canceled.
    1 context sentence
    Summary · context
    STAT3 was silenced by gene transfection technology to verify the core role of STAT3 in GHK Cu treatment of UC.
  18. 18LabIn vitro (cells)Mechanism

    After STAT3 silencing with siRNA, the effect of GHK‑Cu on ZO-1 and Occludin protein expression was canceled.

    In plain wordsIn mouse cells, silencing STAT3 removed the effect of GHK‑Cu on the tight junction proteins ZO-1 and Occludin.

    Peptide
    GHK-Cu
    Outcome
    No significant changeGHK-Cu effect on ZO-1 and Occludin after STAT3 silencing
    Study

    mousen: not reported in source

    MCEC and MPM co-culture, siSTAT3
    Outcome group
    Receptor activity and mechanism · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Our findings revealed that after transfection with STAT3-targeting siRNA (siSTAT3), the stimulant effect of GHK-Cu on the healing of MCECs and the effect on the protein expression of ZO-1 and Occludin is canceled.
    1 context sentence
    Summary · context
    STAT3 was silenced by gene transfection technology to verify the core role of STAT3 in GHK Cu treatment of UC.

Studies that did not test the peptide alone2

In this study, GHK-Cu 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 GHK-Cu.

  1. 19LabNot a test of GHK-Cu aloneIn vitro (cells)Mechanism

    After STAT3 silencing with siRNA, siSTAT3 together with GHK‑Cu inhibited the expression of inflammatory factors.

    In plain wordsIn mouse cells, silencing STAT3 together with GHK‑Cu still lowered inflammatory factors.

    Peptide
    GHK-Cu
    Outcome
    DecreaseInflammatory factor expression after STAT3 silencing
    Study

    mousen: not reported in source

    MCEC and MPM co-culture, siSTAT3
    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    Nevertheless, after transfection with siSTAT3, it could inhibit the expression of inflammatory factors in conjunction with GHK-Cu.
    1 context sentence
    Summary · context
    STAT3 was silenced by gene transfection technology to verify the core role of STAT3 in GHK Cu treatment of UC.

    In this study, GHK-Cu 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 GHK-Cu.

  2. 20Computer modelNot a test of GHK-Cu aloneIn silicoMechanism

    Network pharmacology and molecular docking identified SIRT1 as a potential target of GHK‑Cu.

    In plain wordsComputer models predicted SIRT1 as a possible target of GHK‑Cu.

    Peptide
    GHK-Cu
    Outcome
    Not applicablePredicted target SIRT1
    Study

    n: not reported in source

    Network pharmacology and molecular docking
    Outcome group
    Receptor activity and mechanism · Gastrointestinal

    Source sentences

    Summary
    Subsequently, network pharmacology and molecular docking identified SIRT1 as a potential target of GHK-Cu.
    1 context sentence
    Summary · context
    Network pharmacology and molecular docking were used to predict the core targets of GHK Cu in the treatment of UC.

    In this study, GHK-Cu 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 GHK-Cu.

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

Subjects

Terms as the source lists them.

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