Green tea polyphenol (–)-epigallocatechin-3-gallate (EGCG) is a potent antioxidant with protective effects against neurotoxicity. However, it is currently unclear whether EGCG protects neuronal cells against radiation-induced damage. Therefore, the objective of this study was to investigate the effects of EGCG on ultraviolet (UV)-induced oxidative stress and apoptosis in PC12 cells. The effects of UV irradiation included apoptotic cell death, which was associated with DNA fragmentation, reactive oxygen species (ROS) production, enhanced caspase-3 and caspase-9 activity, and poly (ADP-ribose) polymerase cleavage. UV irradiation also increased the Bax/Bcl-2 ratio and mitochondrial pathway-associated cytochrome c expression. However, pretreatment with EGCG before UV exposure markedly decreased UV-induced DNA fragmentation and ROS production. Furthermore, the UV irradiationinduced increase in Bax/Bcl-2 ratio, cytochrome c upregulation, and caspase-3 and caspase-9 activation were each ameliorated by EGCG pretreatment. Additionally, EGCG suppressed UV-induced phosphorylation of p38 and rescued UV-downregulated phosphorylation of ERK. Taken together, these results suggest that EGCG prevents UV irradiationinduced apoptosis in PC12 cells by scavenging ROS and inhibiting the mitochondrial pathways known to play a crucial role in apoptosis. In addition, EGCG inhibits UV-induced apoptosis via JNK inactivation and ERK activation in PC12 cells. Thus, EGCG represents a potential neuroprotective agent that could be applied to prevent neuronal cell death induced by UV irradiation.

Introduction
Materials and Methods
    1. Cell culture, UV irradiation and EGCG treatment
    2. Cell viability based on 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay
    3. Agarose gel electrophoresis for assessment of DNAfragmentation
    4. 4′,6-diamidino-2-phenylindole (DAPI) staining
    5. Detection of ROS production
    6. Western blot analysis
    7. Measurement of caspase activity
Results
    1. Effects of EGCG on cell viability in UV-irradiatedPC12 cells
    2. EGCG ameliorates apoptosis in UV-irradiated PC12cells
    3. EGCG reduces ROS production in UV-irradiated PC12 cells
    4. EGCG regulates the expression of Bcl-2 family andcytochrome c in UV-irradiated PC12 cells
    5. EGCG inhibits the activation of caspase-3 andcaspase-9 in UV-irradiated PC12 cells
    6. EGCG ameliorates UV-induced apoptosis byinhibiting phosphorylation of p38 in PC12 cells
Discussion
Acknowledgements
Conflicts of Interest
References

• Su-Mi Woo(Department of Oral Physiology, Dental Science Research Institute, School of Dentistry, Chonnam National University)
• Yoon-Jung Kim(Department of Oral Physiology, Dental Science Research Institute, School of Dentistry, Chonnam National University)
• Bangrong Cai(School of Pharmacy, Henan University of Traditional Chinese Medicine)
• Sam-Young Park(Department of Oral Physiology, Dental Science Research Institute, School of Dentistry, Chonnam National University)
• Young Kim(Department of Oral Pathology, Dental Science Research Institute, School of Dentistry, Chonnam National University)
• Ok Joon Kim(Department of Oral Pathology, Dental Science Research Institute, School of Dentistry, Chonnam National University)
• In-Chol Kang(Department of Oral Microbiology, Dental Science Research Institute, School of Dentistry, Chonnam National University)
• Won-Jae Kim(Department of Oral Physiology, Dental Science Research Institute, School of Dentistry, Chonnam National University) Correspondence to
• Ji-Yeon Jung(Department of Oral Physiology, Dental Science Research Institute, School of Dentistry, Chonnam National University) Correspondence to