Journal of the Korean Academy of Pediatric Dentistry 2006;33(1):13-24.
Published online February 28, 2006.
Effects of epigallocatechin gallate on $CoCl_2-induced$ apoptosis in PC12 cells
Hyun-Chul Mo1, Nam-Ki Choi1, Seon-Mi Kim1, Won-Jae Kim2, Kyu-Ho Yang1
1
2 
PC12 세포에서 CoCl2유발 세포자멸사에 대한 epigallocatechin-gallate의 역할
모현철1, 최남기1, 김선미1, 김원재2, 양규호1
1전남대학교 치과대학 소아치과학교실
2전남대학교 치과대학 구강생리학교실 및 치의학연구소
Correspondence:  Kyu-Ho Yang, 
Abstract
Neuronal apoptotic events, consequently resulting in neuronal cell death, are occurred in hypoxic/ischemic condition. This cell death has been shown to be accompanied with the production of reactive oxygen species (ROS), which can attack cellular components such as nucleic acids, proteins and phospholipid. However, the underlying mechanisms of apoptosis induced in hypoxic/ischemic condition and its treatment methods are unsettled. Cobalt chloride (CoCl2) has been known to mimic hypoxic condition including the production of ROS. Epigallocatechin gallate (EGCG), a green tea polyphenol, has diverse pharmacologial activities in cell growth and death. This study was aimed to investigate the apoptotic mechanism by CoCL2 and effects of EGCG on CoCl2-induced apoptosis in PC12 cells. Administration of CoCl2 decreased cell survival in dose- and time-dependent manners and induced genomic DNA fragmentation. Treatment with 100μM EGCG for 30 min before PC12 cells were exposed to 150μM CoCl2, being resulted in the cell viability and DNA fragmentation being rescued. CoCl2 caused morphologic changes such as cell swelling and condensed nuclei whereas EGCG attenuated morphologic changes by CoCl2. EGCG suppressed the apoptotic peak and a loss of Δψm induced by CoCl2. CoCl2 decreased Bcl-2 expression but Bax expression was not changed in CoCl2- treated cells. EGCG attenuated the Bcl-2 underexpression by CoCl2. CoCl2 augumented the cytochrome c release from mitochondria into cytoplasm and increased caspase-8, -9 and caspase-3 activity a marker of the apoptotic executing stage. EGCG ameliorated the incruement in caspase-8, -9 and -3 activity, and cytochrome c release by $CoCl_2$ 수식 이미지 NAC (N-acetyl-cysteine), a scavenger of ROS, attenuated $CoCl_2-induced$ 수식 이미지 apoptosis in consistent with those of EGCG. These results suggest that $CoCl_2$ 수식 이미지 induces apoptotic cell death through both mitochondria- and death receptor-dependent pathway and EGCG has neuroprotective effects against $CoCl_2-induced$ 수식 이미지 apoptosis in PC12 cells.
Key Words: Apoptosis, EGCG, Mitochondria dependent pathway, Death receptor dependent pathway
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