E. O. Gutop, N. S. Linkova, E. O. Kozhevnikova, N. V. Fridman, O. M. Ivko, V. Kh. Khavinson
{"title":"AEDG肽对皮肤成纤维细胞诱导衰老模型氧化应激的抑制作用","authors":"E. O. Gutop, N. S. Linkova, E. O. Kozhevnikova, N. V. Fridman, O. M. Ivko, V. Kh. Khavinson","doi":"10.1134/S2079057022020096","DOIUrl":null,"url":null,"abstract":"<p>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 <i>SOD1</i> and <i>TXNRD1</i> 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 <i>NQO1</i> and <i>CATALASE</i> genes in the culture of skin fibroblasts. AEDG peptide promotes the expression of the <i>SOD-1</i>, <i>NQO1</i>, and <i>CATALASE</i> 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.</p>","PeriodicalId":44756,"journal":{"name":"Advances in Gerontology","volume":null,"pages":null},"PeriodicalIF":0.6000,"publicationDate":"2022-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"AEDG Peptide Prevents Oxidative Stress in the Model of Induced Aging of Skin Fibroblasts\",\"authors\":\"E. O. Gutop, N. S. Linkova, E. O. Kozhevnikova, N. V. Fridman, O. M. Ivko, V. Kh. Khavinson\",\"doi\":\"10.1134/S2079057022020096\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>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 <i>SOD1</i> and <i>TXNRD1</i> 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 <i>NQO1</i> and <i>CATALASE</i> genes in the culture of skin fibroblasts. AEDG peptide promotes the expression of the <i>SOD-1</i>, <i>NQO1</i>, and <i>CATALASE</i> 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.</p>\",\"PeriodicalId\":44756,\"journal\":{\"name\":\"Advances in Gerontology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.6000,\"publicationDate\":\"2022-07-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Advances in Gerontology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://link.springer.com/article/10.1134/S2079057022020096\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"GERIATRICS & GERONTOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in Gerontology","FirstCategoryId":"1085","ListUrlMain":"https://link.springer.com/article/10.1134/S2079057022020096","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"GERIATRICS & GERONTOLOGY","Score":null,"Total":0}
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 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.
期刊介绍：
Advances in Gerontology focuses on biomedical aspects of aging. The journal also publishes original articles and reviews on progress in the following research areas: demography of aging; molecular and physiological mechanisms of aging, clinical gerontology and geriatrics, prevention of premature aging, medicosocial aspects of gerontology, and behavior and psychology of the elderly.
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