Mechanism of amyloid β protein induced neuronal cell death: current concepts and future perspectives
Mechanism of amyloid β protein induced neuronal cell death: current concepts and future perspectives
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β淀粉样蛋白诱导神经细胞死亡的机制：当前概念和未来展望
DOI：
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发表时间：
1997
期刊：
影响因子：
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通讯作者：
Y. Sagara
中科院分区：
文献类型：
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作者：
C. Behl;Y. Sagara
β 淀粉样蛋白 (Aβ) 是一种 40 至 43 个氨基酸的肽，与阿尔茨海默病患者大脑中的斑块相关，对培养的神经元具有细胞毒性。许多抗氧化剂可以保护原代中枢神经系统 (CNS) 培养物和克隆细胞系免受 Aβ 毒性，这表明 Aβ 细胞毒性的一种途径会导致自由基损伤。 Aβ 导致细胞内 H2O2 和脂质过氧化物水平升高。 H2O2 降解酶过氧化氢酶可保护细胞免受 Aβ 毒性。因抗 Aβ 毒性而选择的克隆细胞系也会对 H2O2 的细胞溶解作用产生抗性。此外，Aβ 还能诱导 NF-kB 活性，这是一种被认为受氧化应激调节的转录因子。最后，Aβ 诱导的 H2O2 产生和 Aβ 毒性被抑制黄素氧化酶的试剂阻断，表明 Aβ 激活了此类酶的成员。这些结果表明，Aβ 对神经元的细胞毒作用是由自由基对易感细胞的损伤引起的（Behl 等，1994b）。
Amyloid β protein (A β) is a 40 to 43 amino acid peptide which is associated with plaques in the brains of Alzheimer’s patients and is cytotoxic to cultured neurons. A number of antioxidants protect both primary central nervous system (CNS) cultures and clonal cell lines from Aβ toxicity, suggesting that one pathway to Aβ cytotoxicity results in free radical damage. Aβ causes increased levels of H2O2 and lipid peroxides to accumulate in cells. The H2O2 degrading enzyme catalase protects cells from Aβ toxicity. Clonal cell lines selected for their resistance to Aβ toxicity also become resistant to the cytolytic action of H2O2. In addition, Aβ induces NF-kB activity, a transcription factor thought to be regulated by oxidative stress. Finally, Aβ induced H2O2 production and Aβ toxicity are blocked by reagents which inhibit flavin oxidases, suggesting that Aβ activates a member of this class of enzymes. These results show that the cytotoxic action of Aβ on neurons results from free radical damage to susceptible cells (Behl et al., 1994b).
影响因子：
3.9
作者：
ROYALL, JA;ISCHIROPOULOS, H
通讯作者：
ISCHIROPOULOS, H
影响因子：
56.9
作者：
YANKNER, BA;DUFFY, LK;KIRSCHNER, DA
通讯作者：
KIRSCHNER, DA