he accumulation of peptide-bound copper ion produces multiple anti-inflammatory effects that help to stop the actions of sterilizing oxygen radicals and permit the initiation of healing events. GHK-Cu blocks ferritin channels and the release of free (oxidative) iron, thus blocking iron catalyzed lipid peroxidation that occurs after injury. GHK-Cu blocks also interleukin-1 damage to tissue cells.
GHK-Cu released into the blood stream raises the body's production of, and circulating blood concentration of, wound macrophages that enhance repair.
GHK-Cu suppresses the synthesis of scar development by repressing fibroblast production of TGF-beta-1.
GHK-Cu also chemoattracts wound macrophages to the wound area. These macrophages act directly to stimulate healing by removing cellular debris and secreting a family of approximately 20 growth factor proteins.
GHK-Cu acts directly on fibroblasts to stimulate m-RNAs for collagen, elastin, proteoglycans, metalloproteinases, and TIMP-1 and TIMP-2. This in turn raises the levels of these proteins. This results in a condition whereby protein synthesis and deposition is occurring concomitant with protein breakdown that removes scar tissue and cellular debris remaining from the tissue disruption. Thus, GHK-Cu links scar reduction and the rebuilding of tissues.
GHK-Cu induces angiogenesis by serving as a chemoattractant to direct new blood capillaries to the wound area and by inducing the production of several protein essential for angiogenesis.
10. GHK-Cu induces neuronal outgrowth and re-innervation of the damaged tissues.
Supplier: Erythrulose, kojic dipalmitate, L-erythrulose, kojic acid dipalmitate,a-arbutin, Copper peptide, alpha-arbutin, sodium hyaluronate, hyaluronic acid, arbutin, PT-40, EGF, aFGF, ciclopirox olamine, Epidermal Growth Factor, 3-hydroxypyridine
