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Phosphatidylinositol-3 kinase/Akt and GSK-3 mediated cytoprotective effect of epigallocatechin gallate on oxidative stress-injured neuronal-differentiated N18D3 cells.

Authors
Koh, SH; Kim, SH; Kwon, H; Kim, JG; Kim, JH; Yang, KH; Kim, J; Kim, SU; Yu, HJ; Do, BR; Kim, KS; Jung, HK
Citation
Neurotoxicology, 25(5):793-802, 2004
Journal Title
Neurotoxicology
ISSN
0161-813X1872-9711
Abstract
Epigallocatechin gallate (EGCG) is one of most famous compounds of green tea. EGCG suppresses apoptosis induced by oxidative radical stress through several mechanisms. This study was designed to investigate whether EGCG plays a cytoprotective role by activating phosphatidylinositol-3 kinase (PI3K)/Akt-dependent anti-apoptotic pathway and inhibiting glycogen synthase kinase-3 (GSK-3) activity in oxidative stressed N18D3 neural cells. N18D3 cells, mouse neuroblastoma X dorsal root ganglion hybrid cell line, were pre-treated with EGCG or z-VAD-fmk, non-selective caspase inhibitor used as a control substance, for 2 h. The N18D3 cells were then exposed to low concentration of H(2)O(2) (100 microM) for 30 min, and further incubated for 24 h. MTT (3,[4,5-dimethylthiazol]-2-yl) assay and trypan blue staining were used to identify cell viability. Immunoreactivity (IR) of PI3K, Akt, and GSK-3 beta were measured by Western blotting. MTT assay and trypan blue staining showed that EGCG and z-VAD-fmk significantly increased cell viability, and IR of PI3K, phospho-Akt and phospho-GSK-3 beta was significantly increased in the cells treated with EGCG, but not in z-VAD-fmk treated. These results imply that EGCG has neuroprotective effect by increasing PI3K/Akt-dependent anti-apoptotic signals.
MeSH terms
Amino Acid Chloromethyl Ketones/pharmacologyAnimalsApoptosis/drug effectsBlotting, WesternCaspases/antagonists & inhibitorsCatechin/*analogs & derivatives/*pharmacologyCell Differentiation/drug effectsCell LineCell Survival/drug effectsEnzyme Inhibitors/pharmacologyGlycogen Synthase Kinase 3/*physiologyHydrogen Peroxide/pharmacologyMiceMice, Inbred BALB CNeurons/drug effects/*physiology/ultrastructureNeuroprotective Agents/*pharmacologyOncogene Protein v-aktOxidants/pharmacologyOxidative Stress/drug effects/*physiologyPhosphatidylinositol 3-Kinases/*physiologyRetroviridae Proteins, Oncogenic/*physiologySignal Transduction/drug effects
DOI
10.1016/j.neuro.2004.02.001
PMID
15288510
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
AJOU Authors
김, 승업
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