Green tea polyphenol (-)-epigallocatechin-3-gallate prevents ultraviolet-induced apoptosis in PC12 cells
우수미, 김윤정, Cai Bangrong, 박삼영, 김영, 김옥준, 강인철, 김원재, 정지연,
소속 상세정보
우수미 ( Woo Su-Mi ) - Chonnam National University School of Dentistry Department of Oral Physiology
김윤정 ( Kim Yoon-Jung ) - Chonnam National University School of Dentistry Department of Oral Physiology
( Cai Bangrong ) - Henan University of Traditional Chinese Medicine School of Pharmacy
박삼영 ( Park Sam-Young ) - Chonnam National University School of Dentistry Department of Oral Physiology
김영 ( Kim Young ) - Chonnam National University School of Dentistry Department of Oral Pathology
김옥준 ( Kim Ok-Joon ) - Chonnam National University School of Dentistry Department of Oral Pathology
강인철 ( Kang In-Chol ) - Chonnam National University School of Dentistry Department of Oral Microbiology
김원재 ( Kim Won-Jae ) - Chonnam National University School of Dentistry Department of Oral Physiology
정지연 ( Jung Ji-Yeon ) - Chonnam National University School of Dentistry Department of Oral Physiology
Abstract
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.
키워드
Apoptosis; Epigallcatechin; PC12 cells; Radiation
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