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http://dx.doi.org/10.4062/biomolther.2014.006

The Polyphenol Chlorogenic Acid Attenuates UVB-mediated Oxidative Stress in Human HaCaT Keratinocytes  

Cha, Ji Won (School of Medicine and Institute for Nuclear Science and Technology, Jeju National University)
Piao, Mei Jing (School of Medicine and Institute for Nuclear Science and Technology, Jeju National University)
Kim, Ki Cheon (School of Medicine and Institute for Nuclear Science and Technology, Jeju National University)
Yao, Cheng Wen (School of Medicine and Institute for Nuclear Science and Technology, Jeju National University)
Zheng, Jian (School of Medicine and Institute for Nuclear Science and Technology, Jeju National University)
Kim, Seong Min (School of Medicine and Institute for Nuclear Science and Technology, Jeju National University)
Hyun, Chang Lim (School of Medicine and Institute for Nuclear Science and Technology, Jeju National University)
Ahn, Yong Seok (Research Institute of Processing from Jeju Fisher Food, Choung Ryong Fisheries Co., LTD.)
Hyun, Jin Won (School of Medicine and Institute for Nuclear Science and Technology, Jeju National University)
Publication Information
Biomolecules & Therapeutics / v.22, no.2, 2014 , pp. 136-142 More about this Journal
Abstract
We investigated the protective effects of chlorogenic acid (CGA), a polyphenol compound, on oxidative damage induced by UVB exposure on human HaCaT cells. In a cell-free system, CGA scavenged 1,1-diphenyl-2-picrylhydrazyl radicals, superoxide anions, hydroxyl radicals, and intracellular reactive oxygen species (ROS) generated by hydrogen peroxide and ultraviolet B (UVB). Furthermore, CGA absorbed electromagnetic radiation in the UVB range (280-320 nm). UVB exposure resulted in damage to cellular DNA, as demonstrated in a comet assay; pre-treatment of cells with CGA prior to UVB irradiation prevented DNA damage and increased cell viability. Furthermore, CGA pre-treatment prevented or ameliorated apoptosis-related changes in UVB-exposed cells, including the formation of apoptotic bodies, disruption of mitochondrial membrane potential, and alterations in the levels of the apoptosis-related proteins Bcl-2, Bax, and caspase-3. Our findings suggest that CGA protects cells from oxidative stress induced by UVB radiation.
Keywords
Chlorogenic acid; Human keratinocyte; Ultraviolet B; Oxidative stress; Apoptosis;
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