The green tea polyphenol (-)-epigallocatechin gallate attenuates β-amyloid-induced neurotoxicity in cultured hippocampal neurons
The green tea polyphenol (-)-epigallocatechin gallate attenuates β-amyloid-induced neurotoxicity in cultured hippocampal neurons
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DOI：
10.1016/s0024-3205(01)01438-2
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发表时间：
2001-12-21
期刊：
影响因子：
6.1
通讯作者：
Suh, SI
中科院分区：
文献类型：
--
作者：
Choi, YT;Jung, CH;Suh, SI
先前的证据表明，β淀粉样蛋白（β A）蛋白的神经元毒性是通过氧自由基介导的，并且可以通过抗氧化剂和自由基清除剂来减弱。最近的研究表明，绿色茶多酚减少自由基诱导的脂质过氧化。本研究的目的是调查（-）-表没食子儿茶素没食子酸酯（EGCG）是否会预防或减少暴露于β A的培养海马神经元细胞的死亡，因为EGCG作为绿色茶多酚具有有效的抗氧化特性。海马神经元细胞暴露于β A 48小时后，观察到明显的海马神经元损伤，丙二醛（MDA）水平和caspase活性增加。与EGCG共处理细胞以暴露于betaA提高了细胞存活率并降低了MDA水平和caspase活性。促凋亡蛋白（p53和Bax）、Bcl-XL和环氧合酶（考克斯）蛋白与β A诱导的神经元死亡有关。然而，在这项研究中，EGCG的保护作用似乎与p53、Bax、Bcl-XL和考克斯蛋白的调节无关。综上所述，结果表明，表没食子儿茶素没食子酸酯通过清除活性氧对β A诱导的神经元凋亡具有保护作用，这可能有利于预防阿尔茨海默病。(C)2001 Elsevier Science Inc. All rights reserved.
Previous evidence has indicated that the neuronal toxicity of amyloid beta (betaA) protein is mediated through oxygen free radicals and can be attenuated by antioxidants and free radical scavengers. Recent studies have shown that green tea polyphenols reduced free radical-induced lipid peroxidation. The purpose of this study was to investigate whether (-)-epigallocatechin gallate (EGCG) would prevent or reduce the death of cultured hippocampal neuronal cells exposed to betaA because EGCG has a potent antioxidant property as a green tea polyphenol. Following exposure of the hippocampal neuronal cells to betaA for 48 hours, a marked hippocampal neuronal injuries and increases in malondialdehyde (MDA) level and caspase activity were observed. Co-treatment of cells with EGCG to betaA exposure elevated the cell survival and decreased the levels of MDA and caspase activity. Proapoptotic (p53 and Bax), Bcl-XL and cyclooxygenase (COX) proteins have been implicated in betaA-induced neuronal death. However, in this study the protective effects of EGCG seem to be independent of the regulation of p53, Bax, Bcl-XL and COX proteins. Taken together, the results suggest that EGCG has protective effects against betaA-induced neuronal apoptosis through scavenging reactive oxygen species, which may be beneficial for the prevention of Alzheimer's disease. (C) 2001 Elsevier Science Inc. All rights reserved.