首页> 美国卫生研究院文献>Aging (Albany NY) >Swimming exercise stimulates IGF1/ PI3K/Akt and AMPK/SIRT1/PGC1α survival signaling to suppress apoptosis and inflammation in aging hippocampus
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Swimming exercise stimulates IGF1/ PI3K/Akt and AMPK/SIRT1/PGC1α survival signaling to suppress apoptosis and inflammation in aging hippocampus

机译:游泳运动刺激IGF1 / PI3K / Akt和AMPK / SIRT1 /PGC1α的生存信号从而抑制海马衰老中的细胞凋亡和炎症

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摘要

Hippocampus is one of the most vulnerable brain regions in terms of age-related pathological change. Exercise is presumed to delay the aging process and promote health because it seems to improve the function of most of the aging mechanisms. The purpose of this study is to evaluate the effects of swimming exercise training on brain inflammation, apoptotic and survival pathways in the hippocampus of D-galactose-induced aging in SD rats. The rats were allocated to the following groups: (1) control; (2) swimming exercise; (3) induced-aging by injecting D-galactose; (4) induced-aging rats with swimming exercise. The longevity-related AMPK/SIRT1/PGC-1α signaling pathway and brain IGF1/PI3K/Akt survival pathway were significantly reduced in D-galactose-induced aging group compared to non-aging control group and increased after exercise training. The inflammation pathway markers were over-expressed in induced-aging hippocampus, exercise significantly inhibited the inflammatory signaling activity. Fas-dependent and mitochondrial-dependent apoptotic pathways were significantly increased in the induced-aging group relative to the control group whereas they were decreased in the aging-exercise group. This study demonstrated that swimming exercise not only reduced aging-induced brain apoptosis and inflammatory signaling activity, but also enhanced the survival pathways in the hippocampus, which provides one of the new beneficial effects for exercise training in aging brain.
机译:就年龄相关的病理变化而言,海马是最脆弱的大脑区域之一。运动被认为可以延缓衰老过程并促进健康,因为它似乎可以改善大多数衰老机制的功能。这项研究的目的是评估游泳运动训练对D-半乳糖诱导的SD大鼠衰老的海马中脑炎症,凋亡和存活途径的影响。将大鼠分为以下各组:(1)对照组; (2)游泳锻炼; (3)注射D-半乳糖诱导衰老; (4)诱导衰老大鼠进行游泳运动。与非衰老对照组相比,D-半乳糖诱导的衰老组中与寿命有关的AMPK / SIRT1 /PGC-1α信号通路和脑IGF1 / PI3K / Akt生存通路显着降低,并在运动训练后增加。在诱导衰老的海马中炎症通路标志物过表达,运动显着抑制了炎症信号的活动。诱导衰老组的Fas依赖和线粒体依赖的凋亡途径相对于对照组显着增加,而衰老运动组则降低。这项研究表明,游泳运动不仅减少了衰老引起的脑细胞凋亡和炎性信号转导活性,而且还增强了海马的存活途径,这为运动训练对衰老的大脑提供了新的有益作用之一。

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