- 作者： Yen-Jen Sung Chia-Io Cheng Chaio-Sung Chen Hsien-Bin Huang Fong-Lee Huang Pei-Chun Wu Ming-Shi Shiao Huey-Jen Tsay
- 作者服務機構： Institute of Anatomy and Cell Biology, School of Medicine, and Institute of Neuroscience, School of Life Science, Notional Yang-Ming University, Taipei, Department of Neurosurgery, Chi-Mei Foundation Hospital, Tainan, Institute of Molecular Biology, National Chung Cheng University, Chia-Yi, Department of Medical Research and Education, Veterans Gennral Hospital-Taipei, Taipei, Tawan, ROC
- 中文摘要： --
- 英文摘要： Whether reactive oxygen species (ROS) mediate β-amy-loid (Aβ) neurotoxicity remains controversial. NaivePC12 cells (PC12) and nerve growth factor-differentiatedPC12 cells (dPC12) were used to study the role of ROS incell death induced by Aβ . The viability of PC12 anddPC12 cells decreased by 30-40％ after a 48-hour expo-sure to 20μM Aβ . Microscopic examination showedthat Aβ induced necrosis in PC12 cells and apoptosisin dPC12 cells. Vitamin E (100μM) and other antioxi-dants protected PC12 cells, but not dPC12 cells, againstthe cytotoxic effect of Aβ . Since H O has been pro-posed to be involved in Aβ toxicity, the effects of H O onPC12 and dPC12 cells were studied. Differentiated PC12cells appeared to be sgnificantly more resistant to H 0 than naive PC12 cells. These data suggest that ROS maymediate Aβ toxicity in PC12 cells but not in dPC12cells. Because the intracellular levels of ROS were ele-vated during the differentiation of PC12 cells, the base-line levels of ROS in these two model cell types maydetermine the intracellular mediators for Aβ toxicity.Therefore, the protective effects of antioxidants againstAβ may depend upon the redox state of the cells.
- 中文關鍵字： --
- 英文關鍵字： Alzheimer's disease. amyloid. Apoptosis. Reactive oxygen species
