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KMID : 0811720070110050163
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Korean Journal of Physiology & Pharmacology
2007 Volume.11 No. 5 p.163 ~ p.169
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Protein Kinase C-mediated Neuroprotective Action of (－)-epigallocatechin-3-gallate against Aβ1-42-induced Apoptotic Cell Death in SH-SY5Y Neuroblastoma Cells
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Jang Su-Jeong
Jeong Han-Seong
Park Jong-Seong
Park Sung-Jun
Kim Song-Hee
You Kyoung-Wan
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Abstract
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The neurotoxicity of amyloid β (Aβ) is associated with an increased production of reactive oxygen species and apoptosis, and it has been implicated in the development of Alzheimer’s disease. While (-)-epigallocatechin-3-gallate (EGCG) suppresses Aβ-induced apoptosis, the mechanisms underlying this process have yet to be completely clarified. This study was designed to investigate whether EGCG plays a neuroprotective role by activating cell survival system such as protein kinase C (PKC), extracellular-signal-related kinase (ERK), c-Jun N-terminal kinase (JNK), and anti-apoptotic and pro-apoptotic genes in SH-SY5Y human neuroblastoma cells. One μM Aβ1-42 decreased cell viability, which was correlated with increased DNA fragmentation evidenced by DAPI staining. Pre-treatment of SH-SY5Y neuroblastoma cells with EGCG (1μM) significantly attenuated Aβ1-42-induced cytotoxicity. Potential cell signaling candidates involved in this neuroprotective effects were further examined. EGCG restored the reduced PKC, ERK, and JNK activities caused by Aβ1-42 toxicity. In addition, gene expression analysis revealed that EGCG prevented both the Aβ1-42-induced expression of a pro-apoptotic gene mRNA, Bad and Bax, and the decrease of an anti-apoptotic gene mRNA, Bcl-2 and Bcl-xl. These results suggest that the neuroprotective mechanism of EGCG against Aβ1-42-induced apoptotic cell death includes stimulation of PKC, ERK, and JNK, and modulation of cell survival and death genes.
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KEYWORD
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Aβ, Alzheimer’s disease, Apoptosis, (－)-epigallocatechin-3-gallate, PKC
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