Abstract
Ultraviolet (UV) radiation induces DNA damage, oxidative stress, and inflammatory processes in human keratinocytes, resulting in skin inflammation, photoaging, and photocarcinogenesis. Adequate protection of skin against the harmful effects of UV irradiation is essential. Therefore, in this study, we investigated the protective effects of afzelin, one of the flavonoids, against UV irradiation in human keratinocytes and epidermal equivalent models. Spectrophotometric measurements revealed that the afzelin extinction maxima were in the UVB and UVA range, and UV transmission below 376 nm was <10%, indicating UV-absorbing activity of afzelin. In the phototoxicity assay using the 3T3 NRU phototoxicity test (3T3-NRU-PT), afzelin presented a tendency to no phototoxic potential. In addition, in order to investigate cellular functions of afzelin itself, cells were treated with afzelin after UVB irradiation. In human keratinocyte, afzelin effectively inhibited the UVB-mediated increase in lipid peroxidation and the formation of cyclobutane pyrimidine dimers. Afzelin also inhibited UVB-induced cell death in human keratinocytes by inhibiting intrinsic apoptotic signaling. Furthermore, afzelin showed inhibitory effects on UVB-induced release of pro-inflammatory mediators such as interleukin-6, tumor necrosis factor-α, and prostaglandin-E2 in human keratinocytes by interfering with the p38 kinase pathway. Using an epidermal equivalent model exposed to UVB radiation, anti-apoptotic activity of afzelin was also confirmed together with a photoprotective effect at the morphological level. Taken together, our results suggest that afzelin has several cellular activities such as DNA-protective, antioxidant, and anti-inflammatory as well as UV-absorbing activity and may protect human skin from UVB-induced damage by a combination of UV-absorbing and cellular activities.
Highlights
Ultraviolet B (UVB) exposure of the skin results in skin damage characterized by sunburn, induction of cyclobutane pyrimidine dimer (CPD) [1], immunosuppression [2], oxidative stress, and an acute inflammatory response [3,4]
Apoptosis We examined whether the protective effect of afzelin on the UVB-mediated decrease in cell viability was due to inhibiting apoptosis
We examined the changes in the mitochondrial membrane potential and the mitochondrial permeability transition (MPT) using the JC-1 fluorescent probe to determine whether afzelin modulates the MPT after exposure to UVB
Summary
Ultraviolet B (UVB) exposure of the skin results in skin damage characterized by sunburn, induction of cyclobutane pyrimidine dimer (CPD) [1], immunosuppression [2], oxidative stress, and an acute inflammatory response [3,4]. The antioxidant capability of skin is often overwhelmed by overproduction of reactive oxygen species (ROS) and extensive cellular damage, which result in cell death including necrosis and apoptosis. In addition to the generation of ROS, UVB irradiation of the skin may induce acute skin inflammation, but the use of antioxidants overcomes this imbalance. In this regard, defining novel botanical agents capable of ameliorating the adverse effects of ROS has become an important area of research, as primary prevention approaches to skin cancer have proven inadequate for lowering the incidence of skin cancer; emphasizing the need to develop novel skin cancer chemopreventive agents. The use of botanicals as skin care products has recently increased to protect humans against the adverse effects of UV radiation
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