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Peer-reviewedCC BY-NC-NDJournal of biochemical and molecular toxicology

Stemonine Alleviates UVB‐Induced Keratinocyte Senescence by Activating SIRT3

  • Kun Chen1
  • Xudong Yan2
  • Guixiang You2
  • Mingyang Li2
  • Chen Chen1
  • Xiaolan Yu3
  • Jiyi Xia1,4
4 affiliations
  1. 1Department of Technology and Social Service, Dazhou Vocational College of Chinese Medicine, Dazhou City, Sichuan Province, China.
  2. 2School of Pharmacy, Dazhou Vocational College of Chinese Medicine, North Section of Xiniu Avenue, Southwest Vocational Education Park, Dazhou City, Sichuan Province, China.
  3. 3Department of Obstetrics and Gynecology, The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou City, Sichuan Province, China.
  4. 4Dazhou Chinese Medicine Research and Development Center, Dazhou City, Sichuan Province, China.
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Abstract

Ultraviolet B (UVB) radiation is the primary environmental factor contributing to skin damage, largely by accelerating cellular senescence, which leads to impaired skin function and premature aging. Recent studies have indicated that Stemonine, a natural alkaloid, has therapeutic potential owing to its documented biological activities. In this study, we investigated the protective effects of Stemonine on immortalized human keratinocyte cell line HaCaT against UVB-induced cellular senescence and elucidated the underlying mechanisms. Our results demonstrated that Stemonine significantly improved cell viability, attenuated oxidative stress, and ameliorated mitochondrial dysfunction in UVB-irradiated HaCaT cells. Furthermore, Stemonine treatment reduced DNA damage signaling, downregulated key senescence executors such as acetylated p53 and p21, and decreased SA-β-Gal activity. Importantly, Stemonine upregulated both the expression and activity of SIRT3. Crucially, the protective effects of Stemonine were largely abolished upon SIRT3 knockdown, indicating that its actions are mediated via the SIRT3 pathway. These findings suggest that Stemonine is a promising candidate for mitigating UVB-induced skin aging.

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Cite

BibTeXRIS
BibTeX
@article{chen2026stemonine,
  title = {{Stemonine Alleviates UVB‐Induced Keratinocyte Senescence by Activating SIRT3}},
  author = {Kun Chen and Xudong Yan and Guixiang You and Mingyang Li and Chen Chen and Xiaolan Yu and Jiyi Xia},
  journal = {Journal of biochemical and molecular toxicology},
  year = {2026},
  month = oct,
  doi = {10.1002/jbt.71142},
  url = {https://europepmc.org/article/PMC/PMC13718312},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Stemonine Alleviates UVB‐Induced Keratinocyte Senescence by Activating SIRT3
AU  - Kun Chen
AU  - Xudong Yan
AU  - Guixiang You
AU  - Mingyang Li
AU  - Chen Chen
AU  - Xiaolan Yu
AU  - Jiyi Xia
PY  - 2026
DA  - 2026/10/29
JO  - Journal of biochemical and molecular toxicology
DO  - 10.1002/jbt.71142
UR  - https://europepmc.org/article/PMC/PMC13718312
AB  - Ultraviolet B (UVB) radiation is the primary environmental factor contributing to skin damage, largely by accelerating cellular senescence, which leads to impaired skin function and premature aging. Recent studies have indicated that Stemonine, a natural alkaloid, has therapeutic potential owing to its documented biological activities. In this study, we investigated the protective effects of Stemonine on immortalized human keratinocyte cell line HaCaT against UVB-induced cellular senescence and elucidated the underlying mechanisms. Our results demonstrated that Stemonine significantly improved cell viability, attenuated oxidative stress, and ameliorated mitochondrial dysfunction in UVB-irradiated HaCaT cells. Furthermore, Stemonine treatment reduced DNA damage signaling, downregulated key senescence executors such as acetylated p53 and p21, and decreased SA-β-Gal activity. Importantly, Stemonine upregulated both the expression and activity of SIRT3. Crucially, the protective effects of Stemonine were largely abolished upon SIRT3 knockdown, indicating that its actions are mediated via the SIRT3 pathway. These findings suggest that Stemonine is a promising candidate for mitigating UVB-induced skin aging.
SN  - 1095-6670
SN  - 1099-0461
ER  -