Green tea polyphenol (–)-epigallocatechin-3-gallate prevents ultraviolet-induced apoptosis in PC12 cells

서지정보

ㆍ발행기관 : 대한구강생물학회 ㆍ수록지정보 : International Journal of Oral Biology / 45권 / 4호
ㆍ저자명 : Su-Mi Woo, Yoon-Jung Kim, Bangrong Cai, Sam-Young Park, Young Kim, Ok Joon Kim, In-Chol Kang, Won-Jae Kim, Ji-Yeon Jung

목차

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

영어 초록

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.

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