Just what is Livagen, exactly?
Livagen is a peptide used in scientific studies that affect DNA structure immediately. It may relax chromatin, which boosts gene expression and makes cells seem younger.
The immune system’s lymphocytes benefit from taking Livagen. These cells have been shown to activate the immune system and combat illness in the central nervous system, gastrointestinal tract, heart, and other organs. Ongoing studies of Livagen’s effects on pain and aging are promising.
Livagen peptide has structural similarities with Epitalon/Epithalon, which has been shown to have beneficial effects on degenerative diseases of aging. As a result, Livagen peptide advantages work like anti-aging treatments.
Numerous research on Livagen in the elderly demonstrates that it activates many genes in lymphocytes that usually cease reacting as we become older. These findings indicate that Livagen has an immediate impact on DNA in lymphocytes. The immune system relies mainly on these cells.
Some research suggests that Livagen (Lys-Glu-Asp-Ala) is only partially hydrolyzed. Livagen is entirely unaffected by tiny intestinal peptide hydrolases. Livagen inhibits small intestinal glycol-L-leucine dipeptidase activity by 50 percent in vitro. Ribosomal genes were activated by Livagen, as were genes that had been suppressed owing to the age-related condensation of euchromatic regions in chromosomes.
Based on findings, Livagen activates inactive chromatin by modifying heterochromatin and heterochromatinized areas in aging chromosomes. In addition to Puromycin, leupeptin, and D-PAM, Livagen was also shown to be more effective than these other common peptidase inhibitors. Researchers drew Livagen and Epitalon’s dose-inhibitory effect curves, and experts found the IC50 values for the two substances to be 20 and 500 microM, respectively.
Chromatin activation and the Livagen peptide
The effects of the synthetic peptide Livagen on aging cells were investigated, namely its impact on ribosomal gene activity, heterochromatin denaturation parameters, structural C-heterochromatin polymorphism, and facultative heterochromatin variability. Ribosomal genes were activated by Livagen, as were genes that had been suppressed owing to the age-related condensation of euchromatic regions in chromosomes. The data suggest that Livagen activates inactive chromatin by modifying heterochromatin and heterochromatinized areas in aging chromosomes.
Lymphocytes were collected from patients with hypertrophic cardiomyopathy (HCM) and their relatives, and licensed professionals examined the effects of the peptide bioregulator Livagen (Lys-Glu-Asp-Ala). Both alone and in combination, they reacted with cobalt ions on the activity of nucleolar organizer regions (NORs) and the frequency of associations of acrocentric chromosomes.
It has been shown that using Livagen in conjunction with cobalt ions enhances the incidence of big NORs (scoring 2 or higher) in patients and their families. A significant effect of the chemicals under study was a marked increase in the associative activity of acrocentric chromosomes across all experimental groups. Here, Livagen and cobalt ions proved more beneficial.
We infer that under the action of Livagen and cobalt ions on the lymphocytes of HCM patients and their relatives, decondensation of heterochromatinized chromatin occurs, as the activity of NOR is reliant upon the quality of acrocentric chromosome stalk condensation. This may represent a release situation that occurs during the condensation of inactive genes in the studied populations.
These findings have potential therapeutic implications since they provide new information regarding the protective impact of Livagen and Livagen+Cobalt ions on the lymphocytes of HCM patients and their relatives. You can find more information about this topic, here.
