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Updated: Jun 10, 2025
Induction and Validation of Cellular Senescence in Primary Human Cells
Published on: June 20, 2018
Enhanced SIRT1 Activity by Galangin Mitigates UVB-Induced Senescence in Dermal Fibroblasts via p53 Acetylation
Su-Ying Wen1,2,3, Shang-Chuan Ng4, Yen-Tun Chiu4
1Department of Dermatology, Taipei City Hospital, Zhongxing Branch, Taipei 103, Taiwan, ROC.
Abstract:
Human skin aging, a complex process influenced by intrinsic aging and extrinsic photoaging, is marked by the accumulation of reactive oxygen species (ROS) that cause DNA damage, impaired dermal fibroblast function, and wrinkle formation. External stressors, such as ultraviolet (UV) radiation, can trigger cellular senescence. Sirtuin-1 (SIRT1), an NAD+-dependent enzyme in the sirtuin family, plays a crucial role in deacetylating p53, thereby inhibiting its nuclear translocation and reducing skin senescence. Galangin, a flavonoid found in honey and Alpinia officinarum root, has antioxidant and anti-inflammatory properties. This study investigates the protective mechanism of galangin against UVB-induced senescence in human dermal fibroblasts (HDFs) by examining its effects on SIRT1 and its target, acetylated-p53. An in vitro model of UVB-induced senescence using HDFs and an in vivo model using nude mice were employed to assess the dermal protective effects of galangin. The results demonstrate that while UVB exposure does not decrease SIRT1 protein levels, it impairs its enzymatic function. However, galangin treatment counteracts these adverse effects. Additionally, UVB exposure significantly reduces cell viability and upregulates senescence markers like p16, p21, and p53 nuclear transactivation. An increase in senescence-associated β-galactosidase (SA-β-gal) positive cells was observed in UVB-exposed dermal fibroblasts. Galangin treatment mitigates UVB-induced cellular senescence by enhancing SIRT1-mediated p53 deacetylation, thereby inhibiting nuclear translocation and reducing dermal senescence. These findings suggest that galangin is a promising agent for alleviating UVB-induced skin aging and could be a potential component in antiaging cosmetic formulations.
Insights
Galangin protects skin cells from aging by boosting Sirtuin-1 (SIRT1) activity, which reduces damage caused by UV radiation. This flavonoid helps prevent wrinkles and skin senescence, offering a potential antiaging cosmetic ingredient.
Area of Science:
- Dermatology and Cellular Biology
- Biochemistry and Molecular Biology
Background:
- Human skin aging results from intrinsic factors and extrinsic photoaging, characterized by reactive oxygen species (ROS) and cellular senescence.
- Ultraviolet (UV) radiation exposure triggers senescence, impacting dermal fibroblast function and leading to wrinkles.
- Sirtuin-1 (SIRT1) is vital in regulating cellular senescence by deacetylating p53, thus preventing its nuclear translocation.
Purpose of the Study:
- To investigate the protective effects of galangin against UVB-induced senescence in human dermal fibroblasts (HDFs).
- To elucidate the mechanism involving galangin, SIRT1, and acetylated-p53 in mitigating skin aging.
- To evaluate galangin's potential as an antiaging agent in cosmetic formulations.
Main Methods:
- Utilized in vitro models of UVB-induced senescence in HDFs and in vivo models in nude mice.
- Assessed the impact of UVB exposure and galangin treatment on SIRT1 enzymatic activity, p53 acetylation, and senescence markers (p16, p21, p53).
- Quantified cell viability and senescence-associated β-galactosidase (SA-β-gal) activity.
Main Results:
- UVB exposure impaired SIRT1 enzymatic function without altering protein levels, increased p53 acetylation, and upregulated senescence markers (p16, p21, p53).
- Galangin treatment counteracted UVB-induced impairment of SIRT1 function and reduced p53 nuclear translocation and senescence markers.
- UVB exposure decreased cell viability and increased SA-β-gal positive cells, effects mitigated by galangin.
Conclusions:
- Galangin effectively mitigates UVB-induced cellular senescence in human dermal fibroblasts.
- The protective mechanism involves enhancing SIRT1 activity, leading to p53 deacetylation and reduced nuclear translocation.
- Galangin shows promise as a natural ingredient for antiaging cosmetic products to combat UV-induced skin damage.
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