Abstract
Ultraviolet radiation is the major environmental harmful factor that has emotional impact on human skin. The aim of the present study was to determine the mechanism of protection of cyanidin-3-O-glucoside against ultraviolet B (UVB)-induced damage to human HaCaT keratinocytes. Our results show that cyanidin-3-O-glucoside decreased the levels of intracellular reactive oxygen species generated by UVB treatment. Cyanidin-3-O-glucoside also decreased the UVB-augmented levels of the DNA damage indicators phospho-p53 and phospho-ATM/ATR. In addition, cyanidin-3-O-glucoside protected keratinocytes from UVB-induced injury by overturning the disruption of mitochondrial membrane potential and reversing apoptosis. The expression of anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) was attenuated in UVB-exposed cells but restored in UVB/cyanidin-3-O-glucoside-treated cells. Furthermore, expression of the proapoptotic proteins Bcl-2-associated X (Bax) and the key apoptosis executer cleaved caspase-3 were increased in UVB-irradiated cells and decreased in UVB/cyanidin-3-O-glucoside-treated cells. For these reasons, the results demonstrate that cyanidin-3-O-glucoside protects human keratinocytes against UVB-induced oxidative stress and apoptosis. Our study provides a theoretical basis for the use of cyanidin-3-O-glucoside in the fight against light damage.
Highlights
Ultraviolet (UV) radiation from the sun induces several harmful responses, including erythema, immunosuppression, edema, sunburn, hyperplasia, hyperpigmentation, premature aging, and skin cancer (de Gruijl et al, 1993; Fisher et al, 1997; Viertler et al, 2012)
We focused on the effects of ultraviolet B (UVB) radiation, which is absorbed in greater amounts by human keratinocytes than UVA or UVC radiation (Liebel et al, 2012)
Inhibition of electron transport leads to mitochondrial membrane depolarization, a decrease in mitochondrial oxygen uptake, and reduced phosphorylation of ADP to generate ATP, and leads to an increase in reactive oxygen species (ROS) production following the incomplete reduction of molecular oxygen (O2) (Paz et al, 2008)
Summary
Ultraviolet (UV) radiation from the sun induces several harmful responses, including erythema, immunosuppression, edema, sunburn, hyperplasia, hyperpigmentation, premature aging, and skin cancer (de Gruijl et al, 1993; Fisher et al, 1997; Viertler et al, 2012). UVA (320–400 nm) and UVB (280–320 nm) are harmful to human skin. UVA accounts for more than 90% of the total UV radiation reaching the earth’s surface and is constant throughout the year. UVA is considered to play a crucial role in photoaging and causes epidermal hyperplasia, stratum corneum thickening, and synthesis of inflammatory cytokines and matrix metalloproteinases (MMPs) (Wlaschek et al, 1994; Lavker et al, 1995). UVB causes sunburn, sun tanning, pigmented spots, wrinkles, and accelerates skin aging (Lavker et al, 1995)
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