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Biomolecules & Therapeutics ; : 136-142, 2014.
Article in English | WPRIM | ID: wpr-228914

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.


Subject(s)
Humans , Apoptosis , Caspase 3 , Cell Survival , Cell-Free System , Chlorogenic Acid , Comet Assay , DNA , DNA Damage , Electromagnetic Radiation , Hydrogen Peroxide , Keratinocytes , Membrane Potential, Mitochondrial , Oxidative Stress , Reactive Oxygen Species , Superoxides
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