发芽谷物的生理或饮食优势在过去十年中一直是许多讨论的主题。全球消耗了大约2300万吨燕麦,占全球粮食市场相当大的一部分。燕麦幼苗含有更多的蛋白质,β-葡聚糖,游离氨基酸,和酚类化合物比种子。阿尔茨海默病的进行性神经退行性疾病伴随着记忆和认知功能的恶化。这种疾病的关键指标是人脑中淀粉样β蛋白(或Aβ)的异常积累。在这种情况下,燕麦幼苗提取物(OSE)已被确定为AD的新治疗候选药物,由于其抗氧化活性和AD特异性作用机制。本研究通过检查认知功能和探索炎症反应机制,直接调查OSE如何影响AD及其影响。用研磨机将干燕麦幼苗磨细,插入50%发酵乙醇10次(w/v),并在45℃下搅拌10小时提取。用0.22um过滤器过滤提取物后,其中一些用于UHPLC分析。结果表明,用OSE处理保护BV2细胞免受Aβ25-35诱导的细胞毒性。Tg-5XfadAD小鼠在整个大脑中都有强烈的Aβ沉积,而WT小鼠在他们的大脑中没有表现出任何这样的沉积。观察到数量急剧减少,以及尺寸,暴露于OSE的Tg-5XfadAD小鼠中的Aβ斑块。这项研究表明OSE对神经变性的神经保护作用,突触功能障碍,和β淀粉样蛋白诱导的神经炎症。我们的结果表明,OSE作为一种神经保护剂来对抗AD特异性凋亡细胞死亡,神经炎症,β淀粉样蛋白的积累,以及AD小鼠大脑的突触功能障碍。此外,研究表明,OSE治疗会影响JNK/ERK/p38MAPK信号传导,在p-JNK中具有相当大的抑制作用,在OSE处理的Tg-5XfadAD小鼠的脑中观察到的p-p38和p-ERK水平。
The physiological or dietary advantages of germinated grains have been the subject of numerous discussions over the past decade. Around 23 million tons of oats are consumed globally, making up a sizeable portion of the global grain market. Oat seedlings contain more protein, beta-glucan, free amino acids, and phenolic compounds than seeds. The progressive neurodegenerative disorder of Alzheimer\'s is accompanied by worsening memory and cognitive function. A key indicator of this disorder is the unusual buildup of amyloid-beta protein (or Aβ) in human brains. In this context, oat seedling extract (
OSE) has been identified as a new therapeutic candidate for AD, due to its antioxidant activity and AD-specific mechanism of action. This study directly investigated how
OSE affected AD and its impacts by examining the cognitive function and exploring the inflammatory response mechanism. The dried oat seedlings were grounded finely with a grinder, inserted with 50% fermented ethanol 10 times (w/v), and extracted by stirring for 10 h at 45 °C. After filtering the extract by 0.22 um filter, some of it was used for UHPLC analysis. The results indicated that the treatment with
OSE protects against Aβ25-35-induced cytotoxicity in BV2 cells. Tg-5Xfad AD mice had strong deposition of Aβ throughout their brains, while WT mice did not exhibit any such deposition within their brains. A drastic reduction was observed in terms of numbers, as well as the size, of Aβ plaques within Tg-5Xfad AD mice exposed to OSE. This study indicated
OSE\'s neuroprotective impacts against neurodegeneration, synaptic dysfunction, and neuroinflammation induced by amyloid-beta. Our results suggest that OSE acts as a neuroprotective agent to combat AD-specific apoptotic cell death, neuroinflammation, amyloid-beta accumulation, as well as synaptic dysfunction in AD mice\'s brains. Furthermore, the study indicated that OSE treatment affects JNK/ERK/p38 MAPK signaling, with considerable inhibition in p-JNK, p-p38, and p-ERK levels seen in the brain of
OSE-treated Tg-5Xfad AD mice.