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体育运动与活性氧对大脑的复杂作用 被引量:2

The complex role of physical exercise and reactive oxygen species on brain
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摘要 活性氧(ROS)在有氧代谢中以中度水平持续产生,有利于产生氧化还原信号,但数量较大时却能引起氧化损伤和神经退行性病变。由于大脑对ROS敏感度提高,在不同类型神经细胞中保持正常氧化还原状态尤为重要。过去10年的研究充分说明:有规律的运动对大脑功能产生有益影响,并对中风、老年痴呆和帕金森症的预防和治疗起重要作用。然而,研究运动的具体影响似乎又非常复杂,包括通过神经营养因子的神经发生、毛细血管化增加、氧化损伤减少,以及通过蛋白酶和脑啡肽酶的蛋白降解增加。来自我们及其他实验室的数据表明,运动诱导的ROS水平调节对蛋白含量以及脑源性神经营养因子(BDNF)、酪氨酸激酶B(TrkB)、cAMP反应元件结合蛋白(CREB)的表达有重要作用,有利于完善脑功能、增加神经生成。因此,运动诱导的氧化还原状态调节是一种重要方式,运动能通过这一方式造福于大脑功能、增强对氧化应激的抵抗力,协助从氧化应激中恢复、减弱年龄相关的认知能力下降。 Reactive oxygen species (ROS) are continuously generated during aerobic metabolism and at moderate level. They play a role in redox signaling, but in significant concentration they cause oxidative damage and neurodegeneration. Because of the enhanced sensitivity of brain to ROS, it is especially important to maintain the normal redox state in different types of neuron cells. In last decade it became clear that regular exercise beneficially affects brain function, and can play an important preventive and therapeutic role in stroke, Alzheimer, and Parkinson diseases. The effects of exercise appear to be very complex and could include neurogenesis via neurotrophic factors, increased capillariszation, decreased oxidative damage, and increased proteolyfic degradation by proteasome and neprilysin. Data from our and other laboratories indicate that exercise-induced modulation of ROS levels plays a role in the protein content and expression of brain-derived neurotrophic factor, tyrosinerelated kinase B (TrkB), and cAMP response element binding protein, resulting in better function and increased neurogenesis. Therefore, it appears that exercise-induced modulation of the redox state is an important means, by which exercise benefits brain function, increases the resistance against oxidative stress, facilitates recovery from oxidative stress, and attenuates age-associated decline in cognition.
出处 《Journal of Sport and Health Science》 SCIE 2013年第2期87-93,共7页 运动与健康科学(英文)
基金 supported by Hungarian grants(gsl) from ETT 38388,TeT JAP13/02,OTKA(gs2)(K75702),TAMOP-4.2.2/B-10/1-2010-0013 awarded to Z.Radak
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