GHK Basic and Tissue Degeneration, Inflammation, and Anxiety

GHK Basic comes in two varieties: GHK-cu and GHK. GHK, with or without copper, can affect many genes involved in an organism’s stress response and injury, including antioxidant, anti-inflammatory, anti-pain, anti-anxiety, nerve outgrowth, blood vessel growth, anti-cancer action, and tissue remodeling. GHK Basic is a naturally occurring tripeptide with the amino acid sequence glycyl-histidyl-lysine found in human saliva, urine, and plasma.

GHK levels in human plasma are approximately 200 ng/mL at 20 but decline to around 80 ng/mL at 60^[1]. This decrease in GHK level is accompanied by a significant reduction in an organism’s regenerative capacity. Scientific research shows that GHK can aid in infection control, hair growth, wound healing, facial cosmetic use, cognitive health, and cancer.

The Distinctions Between GHK-cu and GHK Basic

As previously stated, GHK and GHK-cu influence numerous genes responsible for an organism’s response to stress and injury, including anti-inflammatory, anti-pain, anti-anxiety, tissue remodeling, antioxidant, nerve outgrowth, blood vessel growth, and anti-cancer actions. Collagen molecules and the SPARC protein house the GHK sequence; injuries caused by protein breakdown cause GHK to be released.

Copper is one of the essential molecules that can benefit the human body. It is a transitional element required by all eukaryotic organisms, including humans and microbes. In its reduced Cu (I) form, copper is an essential co-factor in many biochemical reactions involving electron transfer. Copper oxidation is necessary for robust enzyme functions such as antioxidant defense, blood clotting, cellular respiration, connective tissue formation, and detoxification. Furthermore, copper is essential for neurotransmission, embryonic development, iron metabolism, oxygenation, and most biological processes.

How GHK Basic can Activate DNA Repair Genes

Repair of DNA genes occurs primarily in young and healthy cells; however, as we age, DNA damage accumulates. Rejuvenating the actions of DNA repair genes can help to slow the aging process.

The Function of GHK Basic Peptide in Fibrinogen Synthesis

Fibrinogen consists of alpha, beta, and gamma polypeptide chains. The beta chain gene of fibrinogen is highly suppressed. In the absence of sufficient fibrinogen, fibrinogen will halt because equal amounts of the three polypeptide chains can sufficiently produce fibrinogen. Furthermore, through its interaction with fibrinogen genes, GHK inhibits fibrinogen synthesis by suppressing the production of the inflammatory cytokine interleukin-6 (IL-6), the primary regulator of fibrinogen production^[2]. GHK inhibits IL-6 secretion in skin fibroblasts and IL-6 gene expression in SZ95 sebocytes in cell culture systems. GHK’s effects on the fibrinogen gene and IL-6 secretion wholly suppressed fibrinogen synthesis.

The Functions of GHK Basic Peptide in Ubiquitin/Proteasome System (UPS)

GHK can activate the ubiquitin and proteasome system (UPS), which removes damaged proteins. The activation and stimulation of the UPS eliminate the effects of aging. GHK stimulates the gene expression of 41 UPS genes while suppressing the face of one UPS gene.

The Antioxidant Effect

GHK basic peptide functions as an antioxidant by activating 14 antioxidant genes while suppressing two pro-oxidant genes. GHK reduces free radicals and toxic end products of lipid peroxidation.

The Impacts of GHK Basic on Tissue Repair

GHK can repair tissue damage, making it the peptide’s most studied function. According to research, GHK activities on tissue repair are evident in hair follicles, skin, the stomach, and the lining of the intestine.
GHK basic peptide, according to Campbell et al., resets the gene expression of fibroblasts from COPD patients into the category of tissue repair by the TGF beta superfamily^[3]. According to Campbell et al., GHK directly stimulates TGF beta and other members of the TGF family that activate the repair process.

The Impacts on Cancer Controlling Genes

Cancer suppression requires DNA repair genes, caspases, and growth regulatory genes. In 2010, Hong et al. discovered 54 genes associated with aggressive, metastatic human colon cancer^[4]. The results showed that two skin remodeling and wound healing molecules, GHK at one micromolar and securinine at 18 micromolar, significantly change the gene expressions and may have a therapeutic impact on patients prone to metastasis.

GHK Basic Effect on Insulin and Insulin-Like Genes

Scientists view the insulin family as a negative controller of longevity; abnormally high insulin levels and insulin-like proteins reduce lifespan. GHK activates three insulin genes and suppresses six others in the system. Furthermore, many organisms’ insulin/IGF-1 receptor pathway contributes to biological aging. In vitro shows that mutations that reduce insulin/IGF-1 signaling slow the degenerative aging process and increase lifespan in organisms such as humans and mice.

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References

1. Dou Y, Lee A, Zhu L, Morton J, Ladiges W. The potential of GHK as an anti-aging peptide. Aging Pathobiol Ther. 2020 Mar 27;2(1):58-61. doi: 10.31491/apt.2020.03.014. PMID: 35083444; PMCID: PMC8789089.
2. Pickart L, Margolina A. Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data. Int J Mol Sci. 2018 Jul 7;19(7):1987. doi: 10.3390/ijms19071987. PMID: 29986520; PMCID: PMC6073405.
3. Campbell JD, McDonough JE, Zeskind JE, Hackett TL, Pechkovsky DV, Brandsma CA, Suzuki M, Gosselink JV, Liu G, Alekseyev YO, Xiao J, Zhang X, Hayashi S, Cooper JD, Timens W, Postma DS, Knight DA, Lenburg ME, Hogg JC, Spira A. A gene expression signature of emphysema-related lung destruction and its reversal by the tripeptide GHK. Genome Med. 2012 Aug 31;4(8):67. doi: 10.1186/gm367. PMID: 22937864; PMCID: PMC4064320.
4. Hong Y, Downey T, Eu KW, Koh PK, Cheah PY. A ‘metastasis-prone’ signature for early-stage mismatch-repair proficient sporadic colorectal cancer patients and its implications for possible therapeutics. Clin Exp Metastasis. 2010 Feb;27(2):83-90. doi: 10.1007/s10585-010-9305-4. Epub 2010 Feb 9. PMID: 20143136.