کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
30835 | 44507 | 2012 | 7 صفحه PDF | دانلود رایگان |
Ultraviolet B (UVB) radiation on human skin induces pathophysiological processes such as oxidative stress and inflammation. In previous reports, the antioxidant effects of triphlorethol-A were shown to protect cells against hydrogen peroxide-induced cell damage and gamma ray-induced oxidative stress. In this study, the role of triphlorethol-A in protecting human keratinocytes (HaCaT) against UVB-induced cell damage was investigated. Triphlorethol-A-treated cells were irradiated with UVB (150 mJ/cm2). Triphlorethol-A decreased UVB-induced intracellular ROS and restored the activities of antioxidant enzymes decreased by UVB radiation. Triphlorethol-A decreased UVB damage to cellular components, such as lipid membrane and DNA, restored cell viability and reduced UVB-induced apoptosis by inhibiting the mitochondria-mediated caspase pathway. Triphlorethol-A also reduced the UVB-induced loss of ΔΨm and the active forms of caspase 9 and caspase 3. The anti-apoptotic effect of triphlorethol-A was found to involve the inhibition of c-Jun NH2-terminal kinase, which was induced by UVB exposure. And triphlorethol-A showed an absorptive capacity at range of UVB.These results suggest that triphlorethol-A protects human keratinocytes against UVB by enhancing the activities of the antioxidant system, inhibiting cellular damage and absorbing the UVB.
► Triphlorethol-A decreased UVB-induced intracellular ROS.
► Triphlorethol-A restored the activities of antioxidant enzymes decreased by UVB.
► Triphlorethol-A decreased UVB damage to cellular components and apoptosis.
► Triphlorethol-A protected human keratinocytes against UVB-induced oxidative stress.
Journal: Journal of Photochemistry and Photobiology B: Biology - Volume 106, 5 January 2012, Pages 74–80