Protective effect of (-)-epigallocatechin gallate against advanced glycation endproducts-induced injury in neuronal cells
Protective effect of (-)-epigallocatechin gallate against advanced glycation endproducts-induced injury in neuronal cells
复制标题
DOI：
10.1248/bpb.30.1369
复制
发表时间：
2007-08-01
影响因子：
2
通讯作者：
Lee, Kwang-Won
中科院分区：
文献类型：
--
作者：
Lee, Sun-Joo;Lee, Kwang-Won
晚期糖基化终产物（AGEs）被认为是与多种神经退行性疾病相关的选择性神经元损伤的次要因素。在这项研究中，我们研究了（-）-表没食子儿茶素没食子酸酯（EGCG），绿色茶多酚的主要单体，对AGEs诱导的神经细胞损伤的保护作用。结果表明，EGCG治疗保护免受甘油三酸酯衍生的AGE诱导的神经毒性，这是与细胞内活性氧的增加，以及对细胞内过氧化氢酶（CAT）和超氧化物歧化酶（SOD）的活性下降。EGCG处理也降低丙二醛和羰基水平，和AGEs的形成。处理与10 μ m EGCG上调SOD和CAT水平，而谷胱甘肽过氧化物酶活性降低。此外，发现5 μ M EGCG下调神经元细胞中AGE受体（AGE）的mRNA水平高达2.5倍，如通过真实的时间PCR所确定的。结果表明，表没食子儿茶素没食子酸酯可通过其抗氧化特性以及通过干扰AGEs-β-淀粉样蛋白相互作用介导的途径对AGEs诱导的神经元细胞损伤表现出保护作用，表明这种茶儿茶素对神经退行性疾病具有有益作用。
Advanced glycation endproducts (AGEs) are believed to be secondary factors in the selective neuronal injury associated with several neurodegenerative disorders. In this study, we investigated the protective effects of (-)-epigallocatechin gallate (EGCG), a major monomer of green tea polyphenols, against AGEs-induced damage in neuron cells. The results showed that EGCG treatment protected against glyceraldehyde-derived AGE-induced neurotoxicity, which is associated with an increase in intracellular reactive oxygen species, as well as against decreases in intracellular catalase (CAT) and superoxide dismutase (SOD) activities. EGCG treatment also decreased malondialdehyde and carbonyl levels, and AGEs formation. Treatment with 10 mu m EGCG upregulated SOD and CAT levels, whereas glutathione peroxidase activity was reduced. Furthermore, 5 mu M EGCG was found to down-regulate the mRNA level of the AGE receptor (RAGE) in neuronal cells up to 2.5 fold, as determined by real time PCR. The results demonstrated that EGCG may exhibit protective effects against AGEs-induced injury in neuronal cells through its antioxidative properties, as well as by interfering with AGEs-RAGE interaction mediated pathways, suggesting a beneficial role for this tea catechin against neurodegenerative diseases.