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木樨草素作为阿尔茨海默病潜在的预防和治疗候选药物。

Luteolin as a potential preventive and therapeutic candidate for Alzheimer's disease.

机构信息

Department of Food Science and Engineering, Ewha Womans University, 52, Ewhayeodae-gil, Seodaemun-gu, Seoul 03760, Republic of Korea.

出版信息

Exp Gerontol. 2017 Sep;95:39-43. doi: 10.1016/j.exger.2017.05.014. Epub 2017 May 17.

DOI:10.1016/j.exger.2017.05.014
PMID:28528007
Abstract

Amyloid cascade hypothesis is the main theoretical framework describing the development of Alzheimer's disease (AD). However, most clinical trials of therapy targeting amyloid-β peptide (Aβ) are unsuccessful because AD is a complex disease involving many genetic and environmental factors. Among various factors, inflammation within the brain in particular has been implicated in the pathogenesis and progression of AD. Furthermore, it has been shown that systemic inflammation can initiate AD. Therefore, anti-inflammatory agents might be beneficial for prevention and/or treatment of AD. Many reports have indicated that luteolin, a flavone found in various foods, has preventive and therapeutic value for neurodegenerative diseases including AD. Such effect of luteolin has been linked to its ability to relieve neuroinflammation. Luteolin also has other biological functions, including antioxidant activity that may provide added benefit for prevention of AD. The exact mechanisms of inflammatory pathways involved in AD pathogenesis need to be further understood to utilize luteolin and many other available anti-inflammatory agents to prevent and treat AD. In addition, it is critical to develop better experimental models that resemble the inflammatory conditions in clinical AD.

摘要

淀粉样蛋白级联假说(amyloid cascade hypothesis)是描述阿尔茨海默病(AD)发展的主要理论框架。然而,大多数针对淀粉样β肽(Aβ)的治疗靶点的临床试验都失败了,因为 AD 是一种涉及许多遗传和环境因素的复杂疾病。在各种因素中,大脑内的炎症尤其与 AD 的发病机制和进展有关。此外,已经表明全身炎症可以引发 AD。因此,抗炎剂可能有益于 AD 的预防和/或治疗。许多报告表明,叶黄素,一种存在于各种食物中的类黄酮,对包括 AD 在内的神经退行性疾病具有预防和治疗价值。叶黄素的这种作用与其缓解神经炎症的能力有关。叶黄素还具有其他生物学功能,包括抗氧化活性,这可能为 AD 的预防提供额外的益处。为了利用叶黄素和许多其他可用的抗炎剂来预防和治疗 AD,需要进一步了解参与 AD 发病机制的炎症途径的确切机制。此外,开发更类似于临床 AD 中炎症条件的更好的实验模型至关重要。

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