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首页> 外文期刊>The European Journal of Neuroscience >The interplay between oxidative stress and brain-derived neurotrophic factor modulates the outcome of a saturated fat diet on synaptic plasticity and cognition.
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The interplay between oxidative stress and brain-derived neurotrophic factor modulates the outcome of a saturated fat diet on synaptic plasticity and cognition.

机译:氧化应激与脑源性神经营养因子之间的相互作用调节了饱和脂肪饮食对突触可塑性和认知的影响。

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Abstract A diet high in saturated fat (HF) decreases levels of brain-derived neurotrophic factor (BDNF), to the extent that compromises neuroplasticity and cognitive function, and aggravates the outcome of brain insult. By using the antioxidant power of vitamin E, we performed studies to determine the role of oxidative stress as a mediator for the effects of BDNF on synaptic plasticity and cognition caused by consumption of the HF diet. Male adult rats were maintained on a HF diet for 2 months with or without 500 IU/kg of vitamin E. Supplementation of the HF diet with vitamin E dramatically reduced oxidative damage, normalized levels of BDNF, synapsin I and cyclic AMP-response element-binding protein (CREB), caused by the consumption of the HF diet. In addition, vitamin E supplementation preserved the process of activation of synapsin I and CREB, and reversed the HF-impaired cognitive function. It is known that BDNF facilitates the synapse by modulating synapsin I and CREB, which have been implicated in synaptic plasticity associated to learning and memory. These results show that oxidative stress can interact with the BDNF system to modulate synaptic plasticity and cognitive function. Therefore, studies appear to reveal a mechanism by which events classically related to the maintenance of energy balance of the cell, such as oxidative stress, can interact with molecular events that modulate neuronal and behavioural plasticity.
机译:摘要高饱和脂肪饮食会降低脑源性神经营养因子(BDNF)的水平,从而损害神经可塑性和认知功能,并加剧脑损伤的结果。通过使用维生素E的抗氧化能力,我们进行了研究以确定氧化应激作为BDNF对食用高脂饮食引起的突触可塑性和认知的影响的介质。雄性成年大鼠在有或没有500 IU / kg维生素E的情况下维持HF饮食2个月。向HF饮食补充维生素E可以显着降低氧化损伤,BDNF,突触素I和循环AMP反应因子-的水平正常化。 HF饮食引起的结合蛋白(CREB)。此外,补充维生素E可以保留突触素I和CREB的激活过程,并逆转HF损害的认知功能。已知BDNF通过调节突触素I和CREB促进突触,所述突触素I和CREB已经牵涉到与学习和记忆相关的突触可塑性。这些结果表明氧化应激可以与BDNF系统相互作用,以调节突触可塑性和认知功能。因此,研究似乎揭示了一种机制,通过该机制经典地与维持细胞能量平衡有关的事件(例如氧化应激)可以与调节神经元和行为可塑性的分子事件相互作用。

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