AEDG Peptide Prevents Oxidative Stress in the Model of Induced Aging of Skin Fibroblasts

Ultraviolet (UV) radiation is one of the main environmental factors leading to oxidative stress and accelerated skin aging. AEDG peptide, a regulator of pineal gland functions, has demonstrated geroprotective and antioxidant effects in in vivo and in vitro studies. The aim of this research was to ev...

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Bibliographic Details
Published in:Advances in gerontology 2022-06, Vol.12 (2), p.143-148
Main Authors: Gutop, E. O., Linkova, N. S., Kozhevnikova, E. O., Fridman, N. V., Ivko, O. M., Khavinson, V. Kh
Format: Article
Language:English
Subjects:
Aging
Antioxidants
Autophagy
DNA damage
Enzymes
Extracellular matrix
Fibroblasts
Genes
Geriatrics/Gerontology
Homeostasis
Hydrogen peroxide
Medicine
Medicine & Public Health
Oxidation
Oxidative stress
Peptides
Proteins
Statistical analysis
Tumors
Ultraviolet radiation
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Summary:Ultraviolet (UV) radiation is one of the main environmental factors leading to oxidative stress and accelerated skin aging. AEDG peptide, a regulator of pineal gland functions, has demonstrated geroprotective and antioxidant effects in in vivo and in vitro studies. The aim of this research was to evaluate the effect of AEDG peptide on the expression of genes encoding enzymes of the antioxidant system (NQO1, SOD1, CATALASE, and TRXR) in human skin fibroblasts in a model of accelerated aging induced by UV radiation. The expression of SOD1 and TXNRD1 genes during UV-induced aging of dermal fibroblasts increases by 2 and 1.7 times, respectively. This can be considered as a defense mechanism against oxidative stress caused by UV radiation. Photoaging does not influence the expression of the NQO1 and CATALASE genes in the culture of skin fibroblasts. AEDG peptide promotes the expression of the SOD-1 , NQO1 , and CATALASE genes in dermal fibroblasts exposed to UV radiation by 2.7, 2.6, and 3.2 times, respectively. AEDG peptide can stimulate the expression of these genes via the Keap1/Nrf2 signaling pathway. AEDG peptide might be potentially effective in preventing the accelerated aging of dermal fibroblasts.
ISSN:2079-0570
2079-0589
DOI:10.1134/S2079057022020096