How does GHK-Cu improve hair follicle growth?


Jan 18, 2023
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GHK-Cu potently inhibited DHT, a regulator of hairloss.​

“Reduce DHT formation in the hair follicles – 5-alpha reductase exists in 2 forms; type 1 which function in hair follicles and type 2 which acts in prostate tissue. Follicle damaging DHT is produced in the hair follicles. Pro- pecia (finasteride) inhibits 5-AR throughout the body and improves hair growth. But it works best on the type 2 form, and is best suited for for controlling prostate enlargement. It also must be administered by pills that spread the drug throughout the body. However, increased copper ions in the skin is better at inhibiting the type 1 5-AR that damages hair growth. Sugimoto et al (Sugimoto 1995) found that copper (II) ions could give up to a 90% inhibition of type 1 5-AR. at At 0.12 micrograms copper ion per milliliter, there was a 50% reduction in activity of type 1 alpha reductase but copper (II) ions were 10-fold less active on inhibiting the type 2 prostate type. Thus, copper ions are more specific inhibitors of 5-AR than finasteride." (6)

GHK-Cu Anti-Inflammatory Actions​

"The human tripeptide Glycyl-l-histidyl-l-lysine (GHK) is present in the plasma, saliva, and urine and is used for wound treatment and skin care. It is naturally occurring, nontoxic, and readily forms complexes with copper, regulating its metabolism and improving its bioavailability. GHK tripeptide and its copper (II)-chelated form (GHK-Cu) accelerate the process of regeneration, wound healing, and antioxidant and anti-inflammatory actions. GHK-Cu suppresses inflammation by lowering the level of acute-phase inflammatory cytokines, including TGF-β and TNF-α, and reduces oxidative damage by modulating iron levels. Recent studies have demonstrated an antioxidant and anti-inflammatory role of GHK-Cu to ameliorate skin damage..." (1)

"GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity while decreased TNF-α and IL-6 production through the suppression of NF-κB p65 and p38 MAPK signaling in vitro and in vivo model of ALI. Moreover, GHK-Cu attenuated LPS-induced lung histological alterations, suppressed the infiltration of inflammatory cells into the lung parenchyma in LPS-induced ALI in mice. Taken together, these findings demonstrate that GHK-Cu possesses a protective effect in LPS-induced ALI by inhibiting excessive inflammatory responses..." (1)

“NF-κB p65 activation is associated with alveolar macrophage activity, which is the major source of inflammatory cytokines. Our results demonstrate that GHK-Cu has the ability to inhibit the LPS-induced phosphorylation of NF-κB p65 at Ser536, an event associated with NF-κB activation, as well as the nuclear translocation of NF-κB p65 in macrophages. The therapeutic potential of inhibiting the NF-κB pathway in chronic inflammatory diseases and inflammatory bowel diseases has also been reported.” (1)

GHK-Cu activates inflammatory mast cells, macrophages, and reduces inflammation via antioxidation.​

“These two molecules activate a plethora of remodeling related processes: [1] chemoattraction of repair cells such as macrophages, mast cells, capillary cells; [2] anti-inflammatory actions (suppression of free radicals, thromboxane formation, release of oxidizing iron, transforming growth factor beta-1, tumor necrosis factor alpha and protein glycation while increasing superoxide dismutase, vessel vasodilation, blocking ultraviolet damage to skin keratinocytes and improving fibroblast recovery after X-ray treatments); [3] increases protein synthesis of collagen, elastin, metalloproteinases, anti-proteases, vascular endothelial growth factor, fibroblast growth factor 2, nerve growth factor, neutrotropins 3 and 4, and erythropoietin; [4] increases the proliferation of fibroblasts and keratinocytes; nerve outgrowth, angiogenesis, and hair follicle size.” (2)

...the tripeptide GHK (derived from both collagen Iα2 and secreted protein acidic and rich in cysteine [SPARC]) is chemotactic for monocytes, macrophages, and mast cells and has pro-angiogenic properties." (3)

GHK-Cu triggers wound healing and cell proliferation​

“Compared GHK to known potent chemoattractants and GHK analogs. An implantable device was used for the study of leukocyte chemoattraction in rats for up to 18 days. GHK attracted wound healing immune cells (mast cells, macrophages, polymorphonuclear leukocytes) at about 10exp (-10) M.” (6)

"...GHK downregulated miR-339-5p expression, and overexpression of miR-339-5p partially reversed the anti-apoptotic effects of GHK in SH-SY5Y cells. Our findings suggest that the p38 MAPK pathway is involved in the GHK-induced downregulation of miR-339-5p, and that the miR-339-5p/VEGFA axis plays a role in preventing neuronal apoptosis following ICH injury. ...GHK downregulated miR-339-5p expression, and overexpression of miR-339-5p partially reversed the anti-apoptotic effects of GHK in SH-SY5Y cells." (4)

GHK-Cu reduces iron toxicity:​

“GHK:Cu(2+) reduced iron release from ferritin by 87%. Ferritin in blood plasma can store up to 4500 atoms of iron per protein molecule, which is a well-known catalyst of lipid peroxidation—a chain reaction, which produces a slew of free radicals, leading to DNA, protein and cell membrane damage.”

"When iron levels rise after significant ingestion, transferrin becomes saturated. Excess iron will circulate in the blood as free iron, which is directly toxic to target organs." (5)

Free iron is a potent neurotoxin:​

"Free iron enters cells and concentrates in the mitochondria. This disrupts oxidative phosphorylation, catalyzes lipid peroxidation, forms free radicals, and ultimately leads to cell death.[4]"