| Summary: | 碩士 === 輔仁大學 === 基礎醫學研究所碩士班 === 97 === UV irradiation is one cause of skin aging and skin cancer. Numerous studies have demonstrated UV exposure result in phosphorylation of extracellular signal-regulated kinases (ERK), p38 kinase, and c-Jun NH2-terminal kinases (JNK) mitogen-activated protein kinases (MAPK) in epidermal keratinocytes. Moreover, UV exposure can induce cyclooxygenase-2 (COX-2) expression and lead to skin inflammation and further cause of skin cancer. What is more, UVB induces aquaporin-3 (AQP-3) down-regulation in human skin keratinocytes, influences water transporting, and causes the dehydration of skin. Chrysin, a flavone, has been proved its efficacy on antioxidant, anti-inflammatory and anti-tumor proliferation. In addition, chrysin has been demonstrated its photoprotective effect in UVA-irradiated human dermal fibroblast. However, little attention has been paid on the protective effect against UVB-induced injury in keratinocytes. Therefore, in this study we investigate underlying protective effect of chrysin on UV-induced damage on HaCaT keratinocytes. We found that chrysin significantly increased cell viability and attenuated the phosphorylation of MAPK on HaCaT keratinocytes after exposure to UVA or UVB. Furthermore, chrysin could decrease the COX-2 expression and reduce cell apoptosis after UV exposure. Chrysin also reversed UVB-induced down-regulation of AQP-3. These data demonstrate that chrysin can prevent UV-induced damage and may be beneficial in the prevention of UV-induced skin injury.
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