Niacin protects against UVB radiation-induced apoptosis in cultured human skin keratinocytes

Ultraviolet radiation is an environmental carcinogenic agent that enhances inflammation and immunological reactions in the exposed human skin cells leading to oxidative photoaging of the epidermal and dermal segment. In the present study, we investigated the protective role of ursolic acid (UA) against ultraviolet B (UVB) radiation- induced photoaging an in vitro model of human skin dermal fibroblasts. UA-pretreated human skin dermal fibroblast (HDF) cells were exposed to UVB radiation to evaluated cell viability, reactive oxygen species (ROS), mitochondrial membrane potential, lipid peroxidation, antioxidant status, DNA damage, proinflammatory response, apoptotic induction, and matrix metalloproteinase (MMP) alteration. The UA pretreatment of HDFs mitigated the UVB irradiation-induced cytotoxicity, ROS generation, and mitochondrial membrane potential alteration and lipid peroxidation, depletion of antioxidant status, DNA damage, and apoptotic induction. UA pretreatment of HDFs also attenuated the UVB-induced expression of inflammatory (TNF-α and NF-κB) and apoptotic (p53, Bax, and caspase-3) and MMPs (MMP-2 and MMP-9) and enhanced the Bcl-2 protein levels in 20 μM UA treatment, when compared to concentrations. Hence, these results revealed that UA has the potential to mitigate UVB-induced extracellular damage by interfering with the ROS-mediated apoptotic induction and photoaging senescence and thus is a potential therapeutic agent to protect the skin against UVB-irradiation induced photooxidative damage.

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Ultraviolet Radiation Induced Apoptosis in Human Skin In Vivo

Radiation Protection Dosimetry ◽

10.1093/oxfordjournals.rpd.a033233 ◽

2000 ◽

Vol 91 (1) ◽

pp. 47-50 ◽

Cited By ~ 1

Author(s):

J.M. Sheehan ◽

A.R. Young

Keyword(s):

Ultraviolet Radiation ◽

Human Skin ◽

Radiation Induced ◽

Induced Apoptosis

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Differential expression of selenoproteins by human skin cells and protection by selenium from UVB-radiation-induced cell death

Biochemical Journal ◽

10.1042/bj3320231 ◽

1998 ◽

Vol 332 (1) ◽

pp. 231-236 ◽

Cited By ~ 70

Author(s):

Teresa S. RAFFERTY ◽

Roderick C. McKENZIE ◽

John A. A. HUNTER ◽

A. Forbes HOWIE ◽

John R. ARTHUR ◽

...

Keyword(s):

Cell Death ◽

Human Skin ◽

Sodium Selenite ◽

Human Fibroblasts ◽

Human Keratinocytes ◽

Uvb Radiation ◽

Skin Damage ◽

Skin Cells ◽

Radiation Induced ◽

Human Skin Cells

The generation of reactive oxygen species has been implicated as part of the mechanism responsible for UVB-radiation-induced skin damage. In mice, evidence suggests that increased dietary selenium intake may protect skin from many of the harmful effects of UVB radiation. We sought to determine the selenoprotein profile of cultured human skin cells and whether selenium supplementation could protect keratinocytes and melanocytes from the lethal effects of UVB radiation. Labelling experiments using [75Se]selenite showed qualitative and quantitative differences in selenoprotein expression by human fibroblasts, keratinocytes and melanocytes. This was most noticeable for thioredoxin reductase (60 kDa) and phospholipid glutathione peroxidase (21 kDa); these proteins were identified by Western blotting. Despite these differences, we found that a 24 h preincubation with sodium selenite or selenomethionine protected both cultured human keratinocytes and melanocytes from UVB-induced cell death. With primary keratinocytes, the greatest reduction in cell death was found with 10 nM sodium selenite (79% cell death reduced to 21.7%; P< 0.01) and with 50 nM selenomethionine (79% cell death reduced to 13.2%; P< 0.01). Protection could be obtained with concentrations as low as 1 nM with sodium selenite and 10 nM with selenomethionine. When selenium was added after UVB radiation, little protection could be achieved, with cell death only being reduced from 88.5% to about 50% with both compounds. In all of the experiments sodium selenite was more potent than selenomethionine at providing protection from UVB radiation.

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