GHK-Cu is a naturally prevalent peptide that was first purified from blood plasma. It has been identified in saliva and urine as well. Experimental research in GHK-Cu indicates the peptide has the potential to impact healing and immune functions.[1] The peptide has been studied for mitigating cell aging action, inducing protein synthesis, free-radical damage control, bacterial infection prevention and the function of skin fibroblasts.
MOLECULAR FORMULA: C14H24N6O4
MOLECULAR WEIGHT: 340.38 g/mol
SEQUENCE: Gly-His-LysCu.xHAc
GHK-CU AND SKIN
GHK-Cu is a natural component of blood, studied for its potential impact on dermal regeneration pathways. Research in skin cultures has suggested that GHK may stimulate the synthesis as well as breaking down of collagen, glycosaminoglycans, and other extracellular matrix components like proteoglycans and chondroitin sulfate. The potential appears to be partially mediated through the positive action of GHK-Cu recruitment on fibroblasts, endothelial cells, and immune cells. The peptide appears to attract these cells to the wound site and coordinate their activity in repairing the damage. The peptide has also been researched for its potential modulation of collagen synthesis. Research in the roles of GHK-Cu suggest its actions may be mediated partially via an expression of transforming growth factor Beta. It is likely that the peptide works through various biochemical pathways and may modify gene expression. Studies in mice suggest that GHK-Cu may increase the rate of wound healing in burns to the extent of about 33%.[1] The peptide not only appears to recruit immune cells and fibroblasts to sites of injury, but may promote the development of new blood vessels at these sites.
GHK-CU AND COGNITIVE, NERVOUS SYSTEM FUNCTIONS
The mechanism behind neuronal death, which occurs in degenerative diseases such as Alzheimer’s, is poorly understood. Studies have suggested GHK-Cu’s potential to inhibit loss in neuronal function, involved in such diseases.[2] In these studies, the molecule has been observed to enhance angiogenesis in the nervous system, potentially stimulate nerve outgrowth, and decrease inflammation in the central nervous system. There is further scientific studies supporting the theory that it may alter the expression profiles of pathological genes and help to reset a state of controlled function in dysfunctional systems. Natural GHK-Cu expression is considered to naturally decrease. Some scientists believe that GHK-Cu is possibly neuroprotective against natural insults like gene dysregulation. The peptide has been suggested to protect neurons in rat brains from apoptosis through the well-known miR-339-59/VEGFA pathway, which is considered to be active after brain bleeds and stroke. In the rat models, GHK-Cu was reported to improve the neurological deficits in the brain, reducing swelling, and preventing neuronal death associated with over-expression of miR-339-5p.
GHK-CU AND BACTERIA
GHK-Cu in combination with certain fatty acids may create a potentially antimicrobial compound acting against bacteria and fungi considered to interfere with tissue repair processes. Research in research models of diabetes has suggested that GHK-Cu may exert action, with findings reporting a combination of standard care and GHK-Cu to induce a 40% increase in wound closure and a 27% reduction in infection rates as opposed to control groups.[3] Similar results have also been noted from studies in research models of ischemic wounds. Researchers report that “GHK-Cu improved healing of ischemic wounds and suppresses inflammation by lowering the level of acute-phase inflammatory cytokines such as TGF-beta and TNF-alpha.”
GHK-CU AND LUNGS
Studies in murine models have suggested that GHK-Cu may protect the lungs against fibrosis.[4] The study has also explored the mechanistic action of the peptide. It was observed to modulate TNF-alpha and IL-6 levels, both of which are considered to function as inflammatory molecules and affect the extracellular matrix and smooth muscles of the lungs. The peptide may reduce lung inflammation, thereby enhancing collagen production and preventing fibrotic remodeling. GHK-Cu was also suggested to be effective in murine research models of acute respiratory distress syndrome (ARDS), an inflammatory lung condition that can aggravate very fast and be fatal. ARDS is linked with injury and infection. Once again, the suggested underlying mechanism of the peptide action is by decreasing the expression of TNF-alpha and IL-6.[5]
GHK-CU AND PAIN PERCEPTION
In rat models, the exposure of GHK-Cu was reported to exhibit a concentration-dependent impact on pain-induced behavior. The peptide appeared to deliver analgesic effects mediated through increased levels of the natural painkiller L-lysine.[6] The researchers reported that “It was found the L-lysine residue plays the key role in these effects, because they were observed under the influence of L-lysine [introduction] in [concentrations] close to its equimolar content in the studied tripeptide.” Similar studies have suggested the potential of the peptide to enhance levels of L-arginine, another analgesic amino acid.[7]
Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing. Bodily introduction of any sort is strictly prohibited by law. All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.
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