Astaxanthin Modulates Oxidative Stress, DNA Repair Pathway, and Cell Migration in UV-B Irradiated Human Adipose Tissue-Derived Mesenchymal Stem Cells.
Sevimli M., Kurt H., Sevimli TS.
Laboratory Study, published in Cell Biochem Biophys (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Cell Biochem Biophys (2026)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42033587
- DOI
- 10.1007/s12013-026-02080-6
Abstract (original English)
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 regenerat
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
How we grade evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.