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首页> 外文期刊>Biological & pharmaceutical bulletin >Protective Effect of(-)-Epigallocatechin Gallate against Advanced Glycation Endproducts-Induced Injury in Neuronal Cells
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Protective Effect of(-)-Epigallocatechin Gallate against Advanced Glycation Endproducts-Induced Injury in Neuronal Cells

机译:(-)-表没食子儿茶素没食子酸酯对神经细胞晚期糖基化终产物所致损伤的保护作用

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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-in-duced 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 upregu-lated 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.
机译: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,我们研究了绿茶多酚的主要单体(-)-表没食子儿茶素没食子酸酯(EGCG)的保护作用。结果表明,EGCG处理可防止甘油醛衍生的AGE诱导的神经毒性,这与细胞内活性氧种类的增加以及细胞内过氧化氢酶(CAT)的减少有关EGCG处理还降低了丙二醛和羰基水平以及AGEs的形成.10μMEGCG处理可上调SOD和CAT水平,从而降低了谷胱甘肽过氧化物酶活性。此外,5μM EGCG通过实时荧光定量PCR检测发现,它能下调神经元细胞中AGE受体(RAGE)的mRNA水平至2.5倍。 GCG通过其抗氧化特性以及通过干扰AGEs-RAGE相互作用介导的途径,可能表现出对AGEs诱导的神经元细胞损伤的保护作用,这表明该茶儿茶素对神经退行性疾病具有有益作用。

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