Skip to content

Study · Animal study (in vivo) · mouse · 2022

14 results

Glycyl-L-histidyl-L-lysine-Cu2+ attenuates cigarette smoke-induced pulmonary emphysema and inflammation by reducing oxidative stress pathway.

Zhang Q, Yan L, Lu J, Zhou X

Frontiers in molecular biosciences22 Jul 2022Cited by 9 (Europe PMC)

PMID35936787 (opens in a new tab)PMCIDPMC9354777 (opens in a new tab)DOI10.3389/fmolb.2022.925700 (opens in a new tab)PepBankPUB-35936787
Download PDFPubMedAsk about this study
Jump to 14 results

Summary

Background: Chronic obstructive pulmonary disease (COPD) is a common respiratory disorder manifested as chronic airway inflammation and persistent airflow limitation with the essential mechanism as inflammatory response and oxidative stress induced by toxic exposures such as cigarette smoke (CS). Glycyl-L-histidyl-L-lysine (GHK) is a nontoxic tripeptide involved in the process of healing and regeneration as a natural product. With the combination of Cu(II), glycyl-L-histidyl-L-lysine-Cu2+ (GHK-Cu) improves antioxidative and anti-inflammatory bioavailability, and they might offer potential therapeutic properties for COPD. Thus, the present study aimed to identify the potential effects of GHK-Cu on emphysema induced by cigarette smoke. Methods: In the in vivo experiment, C57BL/6J mice were exposed to CS for 12 weeks to induce pulmonary emphysema. GHK-Cu was injected intraperitoneally at doses of 0.2, 2 and 20 μg/g/day in 100 µl of saline on alternative days from the 1st day after CS exposure. The effects of GHK-Cu on the morphology of CS-induced emphysema, the inflammatory response and oxidative stress were evaluated. The antioxidative effect of GHK-Cu on human alveolar epithelial A549 cells was assessed in vitro. Results: GHK-Cu treatment attenuated the CS-induced emphysematous changes and partially reversed the matrix metalloprotein -9 (MMP-9)/tissue inhibitor of metalloproteinases-1 (TIMP-1) imbalance in the lung tissue. GHK-Cu reduced the inflammation and oxidation by decreasing the expression of inflammatory cytokines (IL-1β and TNF-α) in the bronchoalveolar lavage and the enzymatic activity of MPO and MDA in the lung homogenate while restoring the T-AOC and GSH content. Furthermore, administration of GHK-Cu reversed the increase in NF-κB expression induced by CS and increased the Nrf2 level, as an antioxidant defense component, in mice with chronic CS exposure. In CSE-exposed human alveolar epithelial A549 cells, GHK-Cu also inhibited oxidative stress by suppressing MDA levels and restoring T-AOC and GSH levels, which were modulated by upregulating Nrf2 expression. Conclusion: GHK-Cu treatment attenuated CS-induced emphysema by anti-inflammation by downregulating NF-κB and antioxidation via upregulation of the Nrf2/Keap1 in lung tissues.
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)Efficacy outcome

    In mice exposed to cigarette smoke, GHK‑Cu treatment attenuated emphysematous changes.

    In plain wordsIn mice exposed to cigarette smoke, GHK‑Cu reduced lung damage typical of emphysema.

    Peptide
    GHK-Cu
    Outcome
    DecreaseEmphysematous changes
    Study

    mousen: not reported in source

    Cigarette smoke-induced pulmonary emphysema
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    0.2, 2 and 20 μg/g/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    GHK-Cu treatment attenuated the CS-induced emphysematous changes
    1 context sentence
    Summary · context
    In the in vivo experiment, C57BL/6J mice were exposed to CS for 12 weeks to induce pulmonary emphysema. GHK-Cu was injected intraperitoneally at doses of 0.2, 2 and 20 μg/g/day in 100 µl of saline on alternative days from the 1st day after CS exposure.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to cigarette smoke, GHK‑Cu partially reversed the MMP-9/TIMP-1 imbalance in lung tissue.

    In plain wordsIn mice exposed to cigarette smoke, GHK‑Cu partly corrected a lung enzyme imbalance.

    Peptide
    GHK-Cu
    Outcome
    DecreaseMMP-9/TIMP-1 imbalance in lung tissue
    Study

    mousen: not reported in source

    Cigarette smoke-induced pulmonary emphysema
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    0.2, 2 and 20 μg/g/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    partially reversed the matrix metalloprotein -9 (MMP-9)/tissue inhibitor of metalloproteinases-1 (TIMP-1) imbalance in the lung tissue.
    1 context sentence
    Summary · context
    In the in vivo experiment, C57BL/6J mice were exposed to CS for 12 weeks to induce pulmonary emphysema. GHK-Cu was injected intraperitoneally at doses of 0.2, 2 and 20 μg/g/day in 100 µl of saline on alternative days from the 1st day after CS exposure.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to cigarette smoke, GHK‑Cu decreased IL-1β expression in bronchoalveolar lavage.

    In plain wordsIn mice exposed to cigarette smoke, GHK‑Cu lowered the inflammation signal IL-1β in lung fluid.

    Peptide
    GHK-Cu
    Outcome
    DecreaseIL-1β in bronchoalveolar lavage
    Study

    mousen: not reported in source

    Cigarette smoke-induced pulmonary emphysema
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    0.2, 2 and 20 μg/g/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    decreasing the expression of inflammatory cytokines (IL-1β and TNF-α) in the bronchoalveolar lavage
    1 context sentence
    Summary · context
    In the in vivo experiment, C57BL/6J mice were exposed to CS for 12 weeks to induce pulmonary emphysema. GHK-Cu was injected intraperitoneally at doses of 0.2, 2 and 20 μg/g/day in 100 µl of saline on alternative days from the 1st day after CS exposure.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to cigarette smoke, GHK‑Cu decreased TNF-α expression in bronchoalveolar lavage.

    In plain wordsIn mice exposed to cigarette smoke, GHK‑Cu lowered the inflammation signal TNF-α in lung fluid.

    Peptide
    GHK-Cu
    Outcome
    DecreaseTNF-α in bronchoalveolar lavage
    Study

    mousen: not reported in source

    Cigarette smoke-induced pulmonary emphysema
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    0.2, 2 and 20 μg/g/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    decreasing the expression of inflammatory cytokines (IL-1β and TNF-α) in the bronchoalveolar lavage
    1 context sentence
    Summary · context
    In the in vivo experiment, C57BL/6J mice were exposed to CS for 12 weeks to induce pulmonary emphysema. GHK-Cu was injected intraperitoneally at doses of 0.2, 2 and 20 μg/g/day in 100 µl of saline on alternative days from the 1st day after CS exposure.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to cigarette smoke, GHK‑Cu decreased MPO enzyme activity in lung homogenate.

    In plain wordsIn mice exposed to cigarette smoke, GHK‑Cu lowered MPO, an inflammation enzyme, in lung tissue.

    Peptide
    GHK-Cu
    Outcome
    DecreaseMPO activity in lung homogenate
    Study

    mousen: not reported in source

    Cigarette smoke-induced pulmonary emphysema
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    0.2, 2 and 20 μg/g/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    the enzymatic activity of MPO and MDA in the lung homogenate
    1 context sentence
    Summary · context
    In the in vivo experiment, C57BL/6J mice were exposed to CS for 12 weeks to induce pulmonary emphysema. GHK-Cu was injected intraperitoneally at doses of 0.2, 2 and 20 μg/g/day in 100 µl of saline on alternative days from the 1st day after CS exposure.
  6. 06AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to cigarette smoke, GHK‑Cu decreased MDA, a marker of oxidative damage, in lung homogenate.

    In plain wordsIn mice exposed to cigarette smoke, GHK‑Cu lowered a marker of oxidative damage in lung tissue.

    Peptide
    GHK-Cu
    Outcome
    DecreaseMDA in lung homogenate
    Study

    mousen: not reported in source

    Cigarette smoke-induced pulmonary emphysema
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    0.2, 2 and 20 μg/g/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    the enzymatic activity of MPO and MDA in the lung homogenate
    1 context sentence
    Summary · context
    In the in vivo experiment, C57BL/6J mice were exposed to CS for 12 weeks to induce pulmonary emphysema. GHK-Cu was injected intraperitoneally at doses of 0.2, 2 and 20 μg/g/day in 100 µl of saline on alternative days from the 1st day after CS exposure.
  7. 07AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to cigarette smoke, GHK‑Cu restored total antioxidant capacity (T-AOC) in lung homogenate.

    In plain wordsIn mice exposed to cigarette smoke, GHK‑Cu restored the antioxidant capacity of lung tissue.

    Peptide
    GHK-Cu
    Outcome
    IncreaseT-AOC in lung homogenate
    Study

    mousen: not reported in source

    Cigarette smoke-induced pulmonary emphysema
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    0.2, 2 and 20 μg/g/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    while restoring the T-AOC and GSH content.
    1 context sentence
    Summary · context
    In the in vivo experiment, C57BL/6J mice were exposed to CS for 12 weeks to induce pulmonary emphysema. GHK-Cu was injected intraperitoneally at doses of 0.2, 2 and 20 μg/g/day in 100 µl of saline on alternative days from the 1st day after CS exposure.
  8. 08AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to cigarette smoke, GHK‑Cu restored glutathione (GSH) content in lung homogenate.

    In plain wordsIn mice exposed to cigarette smoke, GHK‑Cu restored the antioxidant glutathione in lung tissue.

    Peptide
    GHK-Cu
    Outcome
    IncreaseGSH content in lung homogenate
    Study

    mousen: not reported in source

    Cigarette smoke-induced pulmonary emphysema
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    0.2, 2 and 20 μg/g/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    while restoring the T-AOC and GSH content.
    1 context sentence
    Summary · context
    In the in vivo experiment, C57BL/6J mice were exposed to CS for 12 weeks to induce pulmonary emphysema. GHK-Cu was injected intraperitoneally at doses of 0.2, 2 and 20 μg/g/day in 100 µl of saline on alternative days from the 1st day after CS exposure.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In mice with chronic cigarette smoke exposure, GHK‑Cu reversed the smoke-induced increase in NF-κB expression.

    In plain wordsIn mice exposed to cigarette smoke, GHK‑Cu reversed a rise in NF-κB, an inflammation switch.

    Peptide
    GHK-Cu
    Outcome
    DecreaseNF-κB expression
    Study

    mousen: not reported in source

    Cigarette smoke-induced pulmonary emphysema
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    0.2, 2 and 20 μg/g/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    administration of GHK-Cu reversed the increase in NF-κB expression induced by CS
    1 context sentence
    Summary · context
    In the in vivo experiment, C57BL/6J mice were exposed to CS for 12 weeks to induce pulmonary emphysema. GHK-Cu was injected intraperitoneally at doses of 0.2, 2 and 20 μg/g/day in 100 µl of saline on alternative days from the 1st day after CS exposure.
  10. 10AnimalAnimal study (in vivo)Mechanism

    In mice with chronic cigarette smoke exposure, GHK‑Cu increased the Nrf2 level.

    In plain wordsIn mice exposed to cigarette smoke, GHK‑Cu raised Nrf2, a part of the body's antioxidant defence.

    Peptide
    GHK-Cu
    Outcome
    IncreaseNrf2 level
    Study

    mousen: not reported in source

    Cigarette smoke-induced pulmonary emphysema
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    0.2, 2 and 20 μg/g/day · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    increased the Nrf2 level, as an antioxidant defense component, in mice with chronic CS exposure
    1 context sentence
    Summary · context
    In the in vivo experiment, C57BL/6J mice were exposed to CS for 12 weeks to induce pulmonary emphysema. GHK-Cu was injected intraperitoneally at doses of 0.2, 2 and 20 μg/g/day in 100 µl of saline on alternative days from the 1st day after CS exposure.
  11. 11LabIn vitro (cells)Efficacy outcome

    In CSE-exposed human alveolar epithelial A549 cells, GHK‑Cu suppressed MDA levels.

    In plain wordsIn cells from the human lung lining, GHK‑Cu lowered a marker of oxidative damage.

    Peptide
    GHK-Cu
    Outcome
    DecreaseMDA level in A549 cells
    Study

    humann: not reported in source

    CSE-exposed A549 human alveolar epithelial cells
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    GHK-Cu also inhibited oxidative stress by suppressing MDA levels
    1 context sentence
    Summary · context
    In CSE-exposed human alveolar epithelial A549 cells
  12. 12LabIn vitro (cells)Efficacy outcome

    In CSE-exposed human alveolar epithelial A549 cells, GHK‑Cu restored T-AOC levels.

    In plain wordsIn cells from the human lung lining, GHK‑Cu restored antioxidant capacity.

    Peptide
    GHK-Cu
    Outcome
    IncreaseT-AOC in A549 cells
    Study

    humann: not reported in source

    CSE-exposed A549 human alveolar epithelial cells
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    restoring T-AOC and GSH levels
    1 context sentence
    Summary · context
    In CSE-exposed human alveolar epithelial A549 cells
  13. 13LabIn vitro (cells)Efficacy outcome

    In CSE-exposed human alveolar epithelial A549 cells, GHK‑Cu restored GSH levels.

    In plain wordsIn cells from the human lung lining, GHK‑Cu restored the antioxidant glutathione.

    Peptide
    GHK-Cu
    Outcome
    IncreaseGSH level in A549 cells
    Study

    humann: not reported in source

    CSE-exposed A549 human alveolar epithelial cells
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    restoring T-AOC and GSH levels
    1 context sentence
    Summary · context
    In CSE-exposed human alveolar epithelial A549 cells
  14. 14LabIn vitro (cells)Mechanism

    In CSE-exposed human alveolar epithelial A549 cells, the antioxidant effects of GHK‑Cu were modulated by upregulating Nrf2 expression.

    In plain wordsIn cells from the human lung lining, GHK‑Cu raised Nrf2, a part of the antioxidant defence.

    Peptide
    GHK-Cu
    Outcome
    IncreaseNrf2 expression in A549 cells
    Study

    humann: not reported in source

    CSE-exposed A549 human alveolar epithelial cells
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    which were modulated by upregulating Nrf2 expression.
    1 context sentence
    Summary · context
    In CSE-exposed human alveolar epithelial A549 cells

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.

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