The Polyphenol Chlorogenic Acid Attenuates UVB-mediated Oxidative Stress in Human HaCaT Keratinocytes.
- Author:
Ji Won CHA
1
;
Mei Jing PIAO
;
Ki Cheon KIM
;
Cheng Wen YAO
;
Jian ZHENG
;
Seong Min KIM
;
Chang Lim HYUN
;
Yong Seok AHN
;
Jin Won HYUN
Author Information
1. School of Medicine and Institute for Nuclear Science and Technology, Jeju National University, Jeju 690-756, Republic of Korea. jinwonh@jejunu.ac.kr
- Publication Type:Original Article
- Keywords:
Chlorogenic acid;
Human keratinocyte;
Ultraviolet B;
Oxidative stress;
Apoptosis
- MeSH:
Apoptosis;
Caspase 3;
Cell Survival;
Cell-Free System;
Chlorogenic Acid*;
Comet Assay;
DNA;
DNA Damage;
Electromagnetic Radiation;
Humans;
Hydrogen Peroxide;
Keratinocytes*;
Membrane Potential, Mitochondrial;
Oxidative Stress*;
Reactive Oxygen Species;
Superoxides
- From:Biomolecules & Therapeutics
2014;22(2):136-142
- CountryRepublic of Korea
- Language:English
-
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.
