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Received Feb 3, 2017; Revised Jun 14, 2017; Accepted Jul 4, 2017
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction
Ultraviolet (UV) radiation often causes various skin diseases [1]. At short-term UV exposure, it could suppress immune function, and at chronic exposure, it could lead to photoaging and/or carcinoma [2, 3]. Skin damage induced by UV irradiation includes photosensitivity, erythema, and DNA damage resulting in invisible changes of cell and gene level [4–6]. These involve alterations in immune response such as increased mast cells, outburst of cytokines by keratinocytes, and suppressed levels of Langerhans cells [7–9]. It is generally known that the skin is the first line of defense in our immune system that causes it to be one of the primary candidates and targets of oxidative stress [10, 11]. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) have a major participation in the pathogenesis of UV-induced skin damage by both direct DNA damage and indirect ROS-mediated oxidative damage [12–14]. Furthermore, the immune dysfunction and ROS would aggravate the skin barrier structure and function, consequently leading to photoaging [15]. With these reports, targeting ROS-induced cellular damage or immune dysfunction in skin barrier is a strategic move to prevent UV-induced skin damage. A plethora of antioxidant agents in different forms are readily available such as cosmetics, inhalant, and foods to reduce UV-induced skin damage [16–20]. However, convenient treatments...