Role of GHK-Cu Peptide in the Improvement of the Growth of Hair Follicle

by | Feb 21, 2021 | Research

GHK-Cu is formed as a result of the affinity of the human peptide, GHK (glycyl-L-histidyl-L-lysine) to the Cu(2+) (Copper 2+). In human body, the GHK-Cu has varied roles like collagen stimulation; anti-inflammatory and anti-oxidant effects; enhancing the activation of wound healing and many more. In addition to these, the GHK-Cu has also been reported to improve the hair growth.

Hair loss regulator, DHT, is influentially inhibited by GHK-Cu

The GHK-Cu peptide reduces the formation of DHT in the hair follicles. There are mainly 2 forms in which the 5-alpha reductase exists: Type 1 that plays a role in the hair follicles and Type 2 that plays a role in the prostate tissue. Throughout the body, 5-alpha Reductase is inhibited by the pro-pecia (finasteride), thereby improving the hair growth. Although, the pro-pecia is more significant for the Type 2 forms, thereby it controls the enlargement of the prostate. The administration is preferred by pills so that the drug spreads in the entire body. However, in context to the Type 1 5-AR, they are better inhibited by the increasing copper ions in the skin, thereby controlling the damage to the hair growth. As per the research conducted by the different researchers, it can be said that copper ions in the concentration of 0.12 micrograms/ml can inhibit the Type 1 5-AR by upto 90%. It is also reported that Type 2 form is less efficiently inhibited by the copper ions. Hence, it can be concluded that in comparison to Fiansteride, the 5-AR is more specifically inhibited by the copper ions.

The Macrophages, Inflammatory Mast Cells are activated by the GHK-Cu and Inflammation is reduced via Antioxidation

A plethora of remodelling related processes is activated by these 2 molecules. The processes include: (1) Repair cells’ chemoattraction like mast cells, macrophages, capillary cells; (2) The anti-inflammatory actions like Thromboxane formation; Vessel vasodilation; Suppression of the free radicals; Oxidizing iron release; Increase in the Superoxide dismutase and the transformation of the growth factor beta-1, alpha-tumor necrosis factor and protein glycation; vasodilation of vessels; protecting skin keratinocytes from ultraviolet damage; improvement of the fibroblast recovery post X-ray treatments; (3) Enhanced proliferation of keratinocytes and fibroblasts, angiogenesis, nerve outgrowth and the size of the hair follicle; (4) Enhanced synthesis of the protein collagen, anti-proteases, elastin, metalloproteinases, fibroblast growth factor, neutrotropins and erythropoietin, nerve growth factor and vascular endothelial growth factor.

The iron toxicity is reduced by GHK-Cu

After significant ingestion, the levels of iron rise, thereby saturating the Transferrin. The excessive iron will circulate as free iron in the blood and will be toxic directly for the target organs. The Ferritin will release the GHK-Cu (2+) reduced iron by 87%. Approximately, 4500 atoms of iron per protein molecules can be stored in Ferritin, a well-recognized catalyst of the lipid peroxidation, thereby producing a slew of free radicals, resulting in the damage of cell membrane, protein and DNA.

Potent neurotoxin – Free iron

The entry of free iron in the cells and its accumulation in the mitochondria will disrupt the process of oxidative phosphorylation, will catalyse the lipid peroxidation forming free radicals and hence, causes cell death.

Cell proliferation and Wound healing

The research by different scientists has shown that the miR-399-5p expression is downregulated by GHK. In the cells, the anti-apoptotic effect of GHK is partially reversed due to the overexpression of miR-399-5p. The research also suggests that the downregulation of miR-339-5p induced by GHK involves the p38 MAPK pathways. The miR-399-5p/ VEGFA have also shown a role in the prevention of neuronal apoptosis as a consequence of the ICH injury.

In the cells, the miR-399-5p expression is downregulated by GHK; the miR-399-5p is overexpressed which reverses the anti-apoptotic effects of GHK.

The anti-Inflammatory Actions of GHK-Cu

The GHK is found in the urine, saliva and plasma of an individual. It is also utilized for the skin care and wound treatment. It occurs naturally, is non-toxic, forms complexes with copper readily, improves the bioavailability and regulates the metabolism of the copper. The copper (II) chelation and the GHK tripeptide, together form the GHK-Cu, which accelerates the processed of wound healing, regeneration, anti-inflammatory actions and anti-oxidant actions.
The level of the TNF-α and TGF-β, the acute phase inflammatory cytokines, is lowered, thereby resulting in the oxidative damage and hence, the suppression of inflammation.
In a research, it was shown that the GHK-Cu treatment increased the superoxide dismutase and decreased the production of the reactive oxygen species. Also the production of IL-6 and TNF-α was decreased as a result of the suppression of the p39 MAPK and NF-κB p65 in-vivo and in-vitro model.
The results of the studies have shown that the LPS-induced phosphorylation of NF- κB p65 is also inhibited by the GHK-Cu. Many studies have also reported that the GHK-Cu can inhibit the NF-κB pathway in inflammatory bowel diseases and chronic inflammatory diseases.

With all these points, it can be concluded that the GHK-Cu has the potential to improve the growth of the Hair Follicle. It reduces the negative effects like inflammation, iron toxicity and promotes the processes like wound healing and cell proliferation.

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