Journal of biochemical and molecular toxicologyOct 29, 2026

Stemonine may reduce skin cell aging caused by UVB light by activating a protective protein

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Nov 2, 2026

Abstract

Stemonine treatment significantly improved cell viability and reduced DNA damage in UVB-irradiated human skin cells.

Ultraviolet B radiation accelerates cellular aging, impairing skin function.
Stemonine, a natural alkaloid, has protective effects against UVB-induced cellular senescence.
Treatment with Stemonine decreased oxidative stress and improved mitochondrial function.
Key markers of cellular aging, such as acetylated p53 and p21, were downregulated after Stemonine treatment.
The protective effects of Stemonine involve the activation of the SIRT3 pathway.

Simplified

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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Stemonine may reduce skin cell aging caused by UVB light by activating a protective protein

Abstract

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