Protective role of N-trans-feruloyltyramine against 尾-amyloid peptide-induced neurotoxicity in rat cultured cortical neurons

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• 作者：Wipawan Thangnipon^a ; ^{grwtn@mahidol.ac.th} ; Nirut Suwanna^a ; Narisorn Kitiyanant^a ; ^b ; Rungtip Soi-ampornkul^c ; Patoomratana Tuchinda^d ; Bamroong Munyoo^d ; Saksit Nobsathian^d
• 关键词：Alzheimer's disease ; Amyloid 尾-peptide ; N-trans-Feruloyltyramine ; Apoptosis ; Reactive oxygen species
• 刊名：Neuroscience Letters
• 出版年：2012
• 期刊代码：52_03043940
• 类别：neu
• 出版时间：4 April, 2012
• 卷：513
• 期：2
• 页码：229-232
• 文件大小：493 K

摘要

Enhanced oxidative stress and inflammation play important roles in the pathogenesis of Alzheimer's disease (AD). Amyloid 尾-peptide (A尾), a major component of amyloid plaques, is considered to have a causal role in the development and progress of AD by being the initiator of a pathological cascade leading to oxidative stress. The present study investigated the effect of N-trans-feruloyltyramine (NTF) purified from Polyalthia suberosa, an alkaloid shown to protect against oxidative stress and cell death. Pre-treatment of rat primary cortical cell cultures with 25-250 渭M NTF significantly attenuated 10 渭M A尾_1-42-induced neuronal death in a dose-dependent manner. Apoptotic cell death was demonstrated morphologically as well as by detection of the presence of activated caspase-3 and Bax, levels of which could be reduced by NTF pre-treatment. NTF also reduced production of reactive oxygen species induced by A尾_1-42. These findings suggest that the protective effect of NTF against A尾_1-42-induced neuronal death might be due to its antioxidative property.