Lycopene attenuates A1–42 secretion and its toxicity in human cell and Caenorhabditis elegans models of Alzheimer disease
Lycopene attenuates A1–42 secretion and its toxicity in human cell and Caenorhabditis elegans models of Alzheimer disease
复制标题
番茄红素可减弱阿尔茨海默病的人体细胞和秀丽隐杆线虫模型中 A1–42 的分泌及其毒性
作者：
李清华
越来越多的证据表明，阿尔茨海默病患者血浆中的番茄红素浓度降低。病(AD)。番茄红素是类胡萝卜素家族的一员，已被确定为抗氧化剂，可减轻氧化损伤，并在几种AD模型中具有神经保护作用。然而，番茄红素是否。阿尔茨海默病的发病机制及其分子基础尚不清楚。在这项研究中，我们发现。番茄红素可以显著延缓a1 - 42转基因秀丽隐杆线虫菌株GMC101的瘫痪。番茄红素处理减少了瑞典突变型SH-SY5Y细胞中A1-42的分泌。人淀粉样蛋白前体蛋白（APPsw）。接下来，我们发现番茄红素可以下调表达。-淀粉样蛋白前体蛋白（APP）在APPsw细胞中的水平。而且，番茄红素处理不能改变。内源性活性氧水平与APPsw细胞凋亡的关系。然而，番茄红素处理。保护appsw细胞免受h2o2诱导的氧化应激和铜诱导的损伤。总的来说,。我们的数据支持升高的番茄红素有助于降低AD的发病机制。我们的研究结果表明，增加神经元中的番茄红素可能是一种减轻发病和发育的新方法。的广告。
Growing evidence suggests concentration of lycopene was reduced in plasma of patients with Alzheimer.disease (AD). Lycopene, a member ofthe carotenoid family, has been identified as an antioxidantto attenuate oxidative damage and has neuroprotective role in several AD models. However, whether lycopene is.involved in the pathogenesis of AD and molecular underpinnings are elusive. In this study, we found that.lycopene can significantly delay paralysis in the A1–42-transgenic Caenorhabditis elegans strain GMC101..Lycopene treatment reduced A1–42 secretion in SH-SY5Y cells overexpressing the Swedish mutant form.of human -amyloid precursor protein (APPsw). Next, we found lycopene can down-regulate expression.level of -amyloid precursor protein(APP) in APPsw cells. Moreover, lycopene treatment can not change.endogenous reactive oxygen species level and apoptosis in APPsw cells. However, lycopene treatment.protected against H2O2-induced oxidative stress and copper-induced damage inAPPsw cells. Collectively,.our data support that elevated lycopene contributes to the lower pathogenesis of AD. Our findings suggest that increasing lycopene in neurons may be a novel approach to attenuate onset and development.of AD.