Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol University, Salaya, Nakhonpathom, Thailand.
Neurosci Lett. 2012 Apr 4;513(2):229-32. doi: 10.1016/j.neulet.2012.02.047. Epub 2012 Feb 24.
Enhanced oxidative stress and inflammation play important roles in the pathogenesis of Alzheimer's disease (AD). Amyloid β-peptide (Aβ), 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 25-250μM NTF significantly attenuated 10μM Aβ(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 Aβ(1-42). These findings suggest that the protective effect of NTF against Aβ(1-42)-induced neuronal death might be due to its antioxidative property.
增强的氧化应激和炎症在阿尔茨海默病（AD）的发病机制中起重要作用。淀粉样β肽（Aβ）是淀粉样斑块的主要成分，被认为是导致氧化应激的病理级联反应的启动者，从而在 AD 的发展和进展中起因果作用。本研究调查了从榕属植物中分离出的 N-反式-阿魏酰酪胺（NTF）的作用，该生物碱已被证明可抵抗氧化应激和细胞死亡。用 25-250μM NTF 预处理大鼠原代皮质细胞培养物可显著减轻 10μM Aβ（1-42）诱导的神经元死亡，呈剂量依赖性。形态学以及通过检测激活的 caspase-3 和 Bax 的存在来证明细胞凋亡性死亡，NTF 预处理可降低 Bax 和 caspase-3 的水平。NTF 还可减少 Aβ（1-42）诱导的活性氧的产生。这些发现表明，NTF 对 Aβ（1-42）诱导的神经元死亡的保护作用可能归因于其抗氧化特性。
