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GHK-Cu

Copper Tripeptide-1, Glycyl-L-Histidyl-L-Lysine Copper, Prezatide Copper

Quick Stats
Studies 149
Trials 1
Score 2
2024 pubmed 3 citations

The glycyl-l-histidyl-l-lysine-Cu<sup>2+</sup> tripeptide complex attenuates lung inflammation and fibrosis in silicosis by targeting peroxiredoxin 6.

Bian. Yiding Y; Deng. Mingming M; Liu. Jia J; Li. Jiaye J; Zhang. Qin Q; Wang. Zilin Z; Liao. Liwei L; Miao. Jinrui J; Li. Ruixia R; Zhou. Xiaoming X; Hou. Gang G

Key Findings

  • GHK‑Cu binds to the antioxidant protein PRDX6
  • Binding reduces oxidative stress in alveolar macrophages
  • Mice given GHK‑Cu showed less lung inflammation and fibrosis after silica exposure
  • No significant systemic toxicity was observed in the mouse study

Practical Outcomes

  • For biohackers, the data hint that GHK‑Cu may have broader anti‑oxidant and anti‑inflammatory effects beyond skin health, but there’s no human dosing guidance or proof of benefit for general longevity or performance. Until clinical trials are done, it’s not ready for a real‑world protocol, though it could be a molecule to watch for future anti‑aging research.

Summary

A study in mice showed that the naturally occurring peptide GHK‑Cu can stick to a protein called PRDX6, lower oxidative stress in lung immune cells, and reduce lung inflammation and scarring caused by silica dust. The treatment didn’t cause obvious side effects in the animals, but the work was done only in a disease model, not in healthy people.

Abstract

Silicosis is the most common type of pneumoconiosis, having a high incidence in workers chronically exposed to crystalline silica (CS). No specific medication exists for this condition. GHK, a tripeptide naturally occurring in human blood and urine, has antioxidant effects. We aimed to investigate the therapeutic effect of GHK-Cu on silicosis and its potential underlying molecular mechanism. An experimental silicosis mouse model was established to observe the effects of GHK-Cu on lung inflammation and fibrosis. Moreover, the effects of GHK-Cu on the alveolar macrophages (AM) were examined using the RAW264.7&#xa0;cell line. Its molecular target, peroxiredoxin 6 (PRDX6), has been identified, and GHK-Cu can bind to PRDX6, thus attenuating lung inflammation and fibrosis in silicosis mice without significant systemic toxicity. These effects were partly related to the inhibition of the CS-induced oxidative stress in AM induced by GHK-Cu. Thus, our results suggest that GHK-Cu acts as a potential drug by attenuating alveolar macrophage oxidative stress. This, in turn, attenuates the progression of pulmonary inflammation and fibrosis, which provides a reference for the treatment of silicosis.

Study Information

Provider

pubmed

Year

2024

Date

2024-06-14T00:00:00.000Z

DOI

10.1016/j.redox.2024.103237

Citations

3

References

35