Since its discovery in plasma, the naturally occurring copper complex GHK-Cu has been detected in several other bodily fluids, including saliva and urine. Copper peptides are tiny pieces of naturally occurring proteins that bind to copper ions very well; these ions are essential for many physiological processes. Studies suggest that GHK-Cu may facilitate wound healing activation, draw immune cells, have antioxidant and anti-inflammatory properties, stimulate skin fibroblasts to synthesize collagen and glycosaminoglycan and encourage the formation of blood vessels.
Data suggests it may be produced after tissue damage and is a feedback signal. To begin with, it seems to have anti-inflammatory and tissue-protective properties, which might help to regulate the oxidative damage that develops after tissue injury. It has been hypothesized to significantly trigger tissue remodeling, removing injured or scarred tissue and replacing it with new tissue. Because GHK-Cu concentrations appear to decrease over time, these properties may diminish. This leads to increased inflammatory responses, carcinogenic processes, and tissue damage.
GHK-Cu Peptide: Mechanism of Action
As a result of its peptide sequence and copper’s alleged capacity to enhance diverse processes, GHK-Cu may act on several pathways. At the location of tissue damage, GHK-Cu has been hypothesized to attract mast cells, macrophages, and other immune cells. These cells release proteins that promote tissue development and healing. Removing scar tissue and replacing it with fresh tissue are two of the many theorized properties of GHK-Cu, as mentioned before. Research suggests its major mechanism of action may be to stimulate fibroblasts to produce more of the repair and maintenance proteins collagen, elastin, proteoglycans, glycosaminoglycans, and decorin. Additionally, it has been theorized to remove damaged tissue proteins by promoting the synthesis of metalloproteases and protease inhibitors. Because TGF-beta may induce scar formation, it may also decrease fibroblast release of the growth factor throughout this phase.
Research suggests another possible property of GHK-Cu may be stimulating chondrocytes in the bone to produce more collagen. This might trigger an upregulation of bone-promoting osteoblastic cell attachment and an expansion of stromal cells in the bone marrow. Additionally, it seems to aid in forming new blood vessels by providing copper during angiogenesis. Investigations purport that the presence of GHK-Cu in the developing tissue might be critical for sustaining cells because angiogenesis cannot occur without adequate copper storage. Data suggests that GHK-Cu may influence the neurological system to maintain normal function, which may enhance neuronal axon development and proliferation. To prevent iron-catalyzed lipid peroxidation after tissue injury, GHK-Cu has been suggested to restrict ferritin channels and the release of free (oxidative) iron, which damages tissues. The skin, hair follicles, linings of the stomach and intestines, bones, hooves, and fingernails all seem to be able to take advantage of this copper peptide-driven tissue regeneration process.
Research in the Lungs
Some specialists have hypothesized that GHK-Cu may be essential for preventing fibrosis and acute lung damage. Much research has attempted to ascertain its function, and the results have been somewhat substantial. The potential to decrease reactive oxygen species (ROS) production, increase superoxide dismutase (SOD) activity, and decrease TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro models of acute lung injury (ALI) was suggested in one study.
In addition, findings imply that GHK-Cu may reduce histological changes in the lung caused by LPS and prevent inflammatory cells from penetrating the lung parenchyma in mice with LPS-induced acute lung injury. This study suggests that GHK-Cu may be a new research candidate for evaluation in the context of Acute Lung Injury and Respiratory Distress Syndrome, as it has been hypothesized to protect against LPS-induced ALI by reducing the body’s inflammatory response. Additionally, GHK-Cu appeared to have decreased interstitial thickness and inflammatory cell infiltration in pulmonary fibrosis research models. As a result, alveolar fluid TNF-alpha and IL-6 levels seemed to drop, and collagen deposition and lung tissue imbalances were greatly improved.
GHK-Cu Peptide and Cancer
Studies suggest that GHK-Cu may mitigate metastatic cancer. One investigation aimed to determine which chemicals may inhibit genes involved in metastasis and which genes were expressed by normal and malignant cells. Utilizing a database including 7,000 genome expression profiles, researchers analyzed 1309 bioactive compounds. Only 2—including GHK-Cu—were suggested to suppress the genes effectively overexpressed in tumor spreading. Gene regulation is one of the most promising areas of research regarding cancer mitigation and prevention. GHK-Cu seems to be an excellent mediator of this system, and more tissue copper may be the secret to maintaining cells’ functionality.
Please note that none of the substances mentioned in this article have been approved for human or animal consumption and should, therefore, only be used by licensed professionals in contained laboratory settings. This article serves educational purposes only.
References
[i] Pickart l; Margolina A. GHK-Copper Peptide in Skin Remodeling and Anti-Aging. SOFW-Journal | 136 | 6-2010.
[ii] Gul, NY; Topal, A; Cangul, IT; Yanik, K (2008). “The effects of topical tripeptide copper complex and helium-neon laser on wound healing in rabbits”. Vet Dermatol. 19 (1): 7–14. doi:10.1111/j.1365-3164.2007.00647.x.
[iii] Pickart L. Compositions for accelerating wound healing in mammals containing cupric salt or complexes with amino acid or peptide. US Patent 5,164,367, 1992.
[iv] Mulder DPM1, Gerit D.; Patt PhD2, Leonard M.; Sanders DPM, Lee; et al. (1994). “Enhanced healing of ulcers in patients with diabetes by topical treatment of glycyl-l-histidyl-l-lysine”. Wound Repair Regen. 2 (4): 259–269. doi:10.1046/j.1524-475X.1994.20406.x.
[v] Gruchlik A., Jurzak M., Chodurek E., Dzierzewicz Z. Effect of Gly-Gly-His, Gly-His-Lys and their copper complexes on TNF-alpha-dependent IL-6 secretion in normal human dermal fibroblasts. Acta. Pol. Pharm. 2012 Nov-Dec;69(6):1303-6.