Abstract
Ultraviolet-B (UVB) is one of the most cytotoxic and mutagenic stresses that contribute to skin damage and aging through increasing intracellular Ca2+ and reactive oxygen species (ROS). Derinat (sodium deoxyribonucleate) has been utilized as an immunomodulator for the treatment of ROS-associated diseases in clinics. However, the molecular mechanism by which Derinat protects skin cells from UVB-induced damage is poorly understood. Here, we show that Derinat significantly attenuated UVB-induced intracellular ROS production and decreased DNA damage in primary skin cells. Furthermore, Derinat reduced intracellular ROS, cyclooxygenase-2 (COX-2) expression and DNA damage in the skin of the BALB/c-nu mice exposed to UVB for seven days in vivo. Importantly, Derinat blocked the transient receptor potential canonical (TRPC) channels (TRPCs), as demonstrated by calcium imaging. Together, our results indicate that Derinat acts as a TRPCs blocker to reduce intracellular ROS production and DNA damage upon UVB irradiation. This mechanism provides a potential new application of Derinat for the protection against UVB-induced skin damage and aging.
Highlights
Ultraviolet radiation (UVR) is the major etiologic factor for skin aging and its associated diseases and symptoms, such as wrinkles, epidermal pigmentation, melanin production and cancers [1]
To explore the effect of Derinat on UVB-induced skin damage, we first defined the effective dose of Derinat for ultraviolet-B (UVB) irradiation in skin cells in vitro using human keratinocytes (KCs) and human dermal fibroblasts (HDF)
KCs pretreated with different concentrations of Derinat for 24 h were irradiated with UVB, followed by conditioning with 15 μg/mL of Derinat for KCs (Figure 1C) and 150 μg/mL of Derinat for HDF
Summary
Ultraviolet radiation (UVR) is the major etiologic factor for skin aging and its associated diseases and symptoms, such as wrinkles, epidermal pigmentation, melanin production and cancers [1]. Because the energy of UVB is sufficient to generate reactive oxygen species (ROS) in living tissue, UVB causes DNA impairment and tumorigenesis in skin associated with intracellular Ca2+ elevation [4,5]. To reconcile fundamental differences between in vivo and in vitro experimental results, we attempted to identify a suitable reagent to study the molecular mechanism by which UVB induces skin damage and aging. Our results revealed that Derinat significantly protected skin cells, and the epidermis of nude mice from UVB-induced damage Taken together, these results suggest that Derinat reduces skin aging by depressing intracellular Ca2+ elevation and may be useful to prevent/treat age-associated diseases/symptoms
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