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| Original Article | |||||
| Dementia and Neurocognitive Disorders 2003: 2: 1: 1-10 | |||||
| SH-SY5Y Human Neuroblastoma Cell에서 에스트로겐의 신경세포 보호효과에 대한 기전 | |||||
|---|---|---|---|---|---|
| 염지현, 김희, 홍현석, 방오영*, 허균*, 묵인희 | |||||
| 아주대학교 의과대학 뇌질환연구센터, 신경과학교실* | |||||
| Neuroprotective Effects of Estrogen in SH-SY5Y Human Neuroblastoma Cells | |||||
| Ji Hyun Yeom, M.D., Hee Kim, M.D., Hyun-Seok Hong, M.D., Oh-Young Band, M.D.*, Kyoon Huh, M.D.*, Inhee Mook-Jung, M.D. | |||||
| Brain Disease Research Center, Department of Neurology*, Ajou University School of Medicine, Suwon, Korea | |||||
| Apoptosis is one major mechanism underlying neuronal cell death in degenerative diseases in the central nervous system. Previous studies have shown that estrogen has neuroprotective effects in several neuronal cell death model systems. In the present study, we established a staurosporine-induced apoptotic neuronal cell death system with human SH-SY5Y cell line. 17bestradiol (E2) blocked staurosporine-induced apoptosis of SH-SY5Y cells, as revealed by MTT as well as LDH assay. The cells showed typical DNA fragmentation at 4 h and 8 h following staurosporine treatment, which was attenuated by E2 pretreatment. Staurosporine-induced chromatin condensation was also reduced by E2 treatment. Because apoptotic stimuli are known to induce caspase-3 activation and PARP cleavage, we examined whether E2 blocks these processes. E2 markedly attenuated staurosporine-induced casapase-3 activation and PARP cleavage. This study shows that E2 blocks staurosporine-induced apoptosis in SH-SY5Y human neuroblastoma cells, suggesting that E2 is a neuroprotective agent that may be used for the treatment of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. | |||||
| Key Words: Alzheimer's disease, Estrogen, Beta amyloid, Caspase-3, Cell death | |||||
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