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<p>Ultraviolet B (UV-B) radiation is a major factor inducing DNA damage, genomic instability, aging, and functional decline in skin cells. Adipose tissue-derived mesenchymal stem cells (AT-MSCs) are widely used in dermatological and regenerative contexts; however, the impact of UV-B on their biological functions and the potential protective advantages of astaxanthin (ASX) are not yet sufficiently elucidated. We aimed to investigate the effects of UV-B on survival, oxidative balance, migratory capacity, DNA damage and expression of DNA repair genes in AT-MSCs and the potential ameliorative effects of ASX. ASX treatment significantly restored oxidative balance, consequently confirming its robust antioxidant capabilities and partially improving impaired cell migration. ASX treatment significantly reduced UV-B-induced DNA damage, an effect demonstrated by a substantial decrease in Olive Tail Moment (OTM), tail length, and % tail DNA parameters. UV-B significantly increased the activity of various DNA double-strand break (DSB) repair genes, including BRCA1, BRCA2, RAD50, RAD51, Ku70, Ku80, XRCC1, and XRCC4.ASX inhibited the overexpression of many genes and enhanced the activity of RAD51. These findings suggest that ASX protects against UV-B-induced genomic and physiological effects. Therefore, ASX may enhance the safety and therapeutic efficacy of MSC-based dermatological and regenerative treatments exposed to UV stress.</p>

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Astaxanthin Modulates Oxidative Stress, DNA Repair Pathway, and Cell Migration in UV-B Irradiated Human Adipose Tissue-Derived Mesenchymal Stem Cells

  • 期刊论文

  • 发表日期：

    2026年4月25日

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  • Murat Sevimli,
  • Hulyam Kurt,
  • Tugba Semerci Sevimli

摘要

Ultraviolet B (UV-B) radiation is a major factor inducing DNA damage, genomic instability, aging, and functional decline in skin cells. Adipose tissue-derived mesenchymal stem cells (AT-MSCs) are widely used in dermatological and regenerative contexts; however, the impact of UV-B on their biological functions and the potential protective advantages of astaxanthin (ASX) are not yet sufficiently elucidated. We aimed to investigate the effects of UV-B on survival, oxidative balance, migratory capacity, DNA damage and expression of DNA repair genes in AT-MSCs and the potential ameliorative effects of ASX. ASX treatment significantly restored oxidative balance, consequently confirming its robust antioxidant capabilities and partially improving impaired cell migration. ASX treatment significantly reduced UV-B-induced DNA damage, an effect demonstrated by a substantial decrease in Olive Tail Moment (OTM), tail length, and % tail DNA parameters. UV-B significantly increased the activity of various DNA double-strand break (DSB) repair genes, including BRCA1, BRCA2, RAD50, RAD51, Ku70, Ku80, XRCC1, and XRCC4.ASX inhibited the overexpression of many genes and enhanced the activity of RAD51. These findings suggest that ASX protects against UV-B-induced genomic and physiological effects. Therefore, ASX may enhance the safety and therapeutic efficacy of MSC-based dermatological and regenerative treatments exposed to UV stress.