Polycyclic phenols, estrogens and neuroprotection: a proposed mitochondrial mechanism
Polycyclic phenols, estrogens and neuroprotection: a proposed mitochondrial mechanism
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DOI：
10.1016/s0531-5565(02)00162-6
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发表时间：
2003-01-01
影响因子：
3.9
通讯作者：
Gordon, K
中科院分区：
文献类型：
--
作者：
Dykens, JA;Simpkins, JW;Gordon, K
多环酚，包括雌激素，已经在各种细胞和动物模型系统中被证明是有效的神经保护剂。虽然经典的雌激素受体相互作用和相应的反应在某些情况下会发挥作用，但不与雌激素受体ERα或ERβ相互作用的多环酚更有可能是通过非基因组机制发挥神经保护作用(S)。我们认为，这种非女性化的多环酚至少部分地通过稳定线粒体，防止与线粒体功能障碍相关的细胞凋亡和/或坏死性死亡来发挥其保护作用。与线粒体模型和现有数据一致，这些化合物保护神经元和其他类型的细胞免受各种病理相关应激源的影响。(C)2002 Elsevier Science Inc.保留所有权利。
Polycyclic phenols, including the estrogens, have been shown to be potent neuroprotectants in a variety of cellular and animal model systems. Although classical estrogen receptor interactions and consequent responses play a role in certain circumstances, the neuroprotective activity of polycyclic phenols that do not interact with estrogen receptors ERalpha or ERbeta is more likely to be through non-genomic mechanism(s). We propose here that such non-feminizing polycyclic phenols exert their protective effects at least in part by stabilizing mitochondria, preventing apoptotic and/or necrotic forms of cell death that are associated with mitochondrial dysfunction. Consistent with this mitochondrial model and the available data, these compounds protect neurons and other cell types from a wide variety of pathologically relevant stressors. (C) 2002 Elsevier Science Inc. All rights reserved.