Molecular Nutrition Group, School of Chemistry, Food and Pharmacy, University of Reading, Reading RG2 6AP, UK.
Proc Nutr Soc. 2010 May;69(2):244-60. doi: 10.1017/S0029665110000054. Epub 2010 Feb 17.
The consumption of flavonoid-rich foods and beverages has been suggested to limit the neurodegeneration associated with a variety of neurological disorders and to prevent or reverse normal or abnormal deteriorations in cognitive performance. Flavonoids mediate these effects via a number of routes, including a potential to protect neurons against injury induced by neurotoxins, an ability to suppress neuroinflammation and a potential to promote memory, learning and cognitive function. Originally, it was thought that such actions were mediated by the antioxidant capacity of flavonoids. However, their limited absorption and their low bioavailability in the brain suggest that this explanation is unlikely. Instead, this multiplicity of effects appears to be underpinned by three separate processes: first, through their interactions with important neuronal and glial signalling cascades in the brain, most notably the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways that regulate pro-survival transcription factors and gene expression; second, through an ability to improve peripheral and cerebral blood flow and to trigger angiogenesis and neurogenesis in the hippocampus; third, by their capacity to directly react with and scavenge neurotoxic species and pro-inflammatory agents produced in the brain as a result of both normal and abnormal brain ageing. The present review explores the potential inhibitory or stimulatory actions of flavonoids within these three systems and describes how such interactions are likely to underlie neurological effects.
富含类黄酮的食物和饮料的消费被认为可以限制与各种神经紊乱相关的神经退行性变，并预防或逆转认知功能的正常或异常恶化。类黄酮通过多种途径介导这些作用，包括保护神经元免受神经毒素诱导的损伤的潜力、抑制神经炎症的能力以及促进记忆、学习和认知功能的潜力。最初，人们认为这些作用是由类黄酮的抗氧化能力介导的。然而，它们在大脑中的吸收有限和生物利用度低表明，这种解释不太可能。相反，这种多种作用似乎是由三个独立的过程支撑的：首先，通过它们与大脑中重要的神经元和神经胶质信号级联的相互作用，特别是调节生存转录因子和基因表达的磷脂酰肌醇 3-激酶/ Akt 和丝裂原活化蛋白激酶途径；其次，通过改善外周和脑血流以及在海马中触发血管生成和神经发生的能力；第三，通过其与在大脑中由于正常和异常脑老化而产生的神经毒性物质和促炎剂直接反应和清除的能力。本综述探讨了类黄酮在这三个系统中的潜在抑制或刺激作用，并描述了这种相互作用如何可能是神经作用的基础。
