DOI QR코드

DOI QR Code

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

  • Woo, Su-Mi (Department of Oral Physiology, Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Kim, Yoon-Jung (Department of Oral Physiology, Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Cai, Bangrong (School of Pharmacy, Henan University of Traditional Chinese Medicine) ;
  • Park, Sam-Young (Department of Oral Physiology, Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Kim, Young (Department of Oral Pathology, Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Kim, Ok Joon (Department of Oral Pathology, Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Kang, In-Chol (Department of Oral Microbiology, Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Kim, Won-Jae (Department of Oral Physiology, Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Jung, Ji-Yeon (Department of Oral Physiology, Dental Science Research Institute, School of Dentistry, Chonnam National University)
  • 투고 : 2020.11.03
  • 심사 : 2020.11.11
  • 발행 : 2020.12.31

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 irradiation-induced 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 irradiation-induced 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.

키워드

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