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自愿运动促进神经营养因子并抑制海马缺血中的细胞凋亡。

Voluntary exercise promotes neurotrophic factor and suppresses apoptosis in hippocampal ischemia.

作者信息

Zhang Zhixiong, Li Rong, Zhang Xiaoyan, Wei Yaxuan, Ma Hongbing, Zhu Ling, Yin Rong

机构信息

Department of Neurology, The 940th Hospital of Joint Logistics Support Force of Chinese People's Liberation Army, No.333 Binhe Road, Qilihe District, Lanzhou City, Gansu Province, 730050, China.

出版信息

J Integr Neurosci. 2019 Mar 30;18(1):65-70. doi: 10.31083/j.jin.2019.01.118.

DOI:10.31083/j.jin.2019.01.118
PMID:31091850
Abstract

Previous studies have demonstrated that exercise facilitates recovery from ischemia. However, the mechanisms need to be further elucidated. The current investigation was designed to study the effect of voluntary exercise on cerebral ischemia and discuss possible mechanisms usingmiddle cerebral artery occlusion model. Rats were randomly allocated to three groups: control, middle cerebral artery occlusion, and middle cerebral artery occlusion plus exercise. The middle cerebral artery occlusion plus exercise group was preconditioned by three weeks of voluntary wheel running prior to surgery. The accelerated rotarod test was employed to evaluate motor performance. Infarct volumes were analyzed to detect the neuroprotective effect of voluntary exercise. Brain-derived neurotrophic factor, Bax, Bcl-2, and caspase-3 protein expressions were measured by Western blot. Behavior evaluation showed the middle cerebral artery occlusion plus exercise group achieved significantly longer time on a rotarod than the unexercised group. Additionally, voluntary exercise reduced cerebral infarction and increased brain derived neurotrophic factor expression. Exercise down-regulated the apoptotic Bax/Bcl-2 ratio and caspase-3 protein expression. Results indicate that voluntary wheel running promote hippocampal brain derived neurotrophic factor and inhibit cell apoptosis in ischemia-induced impairment.

摘要

先前的研究表明,运动有助于从缺血中恢复。然而,其机制仍需进一步阐明。本研究旨在探讨自主运动对脑缺血的影响,并使用大脑中动脉闭塞模型探讨可能的机制。将大鼠随机分为三组:对照组、大脑中动脉闭塞组和大脑中动脉闭塞加运动组。大脑中动脉闭塞加运动组在手术前进行了为期三周的自主轮转运动预处理。采用加速转棒试验评估运动能力。分析梗死体积以检测自主运动的神经保护作用。通过蛋白质免疫印迹法检测脑源性神经营养因子、Bax、Bcl-2和半胱天冬酶-3蛋白的表达。行为评估显示,大脑中动脉闭塞加运动组在转棒上的停留时间明显长于未运动组。此外,自主运动减少了脑梗死,并增加了脑源性神经营养因子的表达。运动下调了凋亡相关的Bax/Bcl-2比值和半胱天冬酶-3蛋白的表达。结果表明,自主轮转运动可促进海马脑源性神经营养因子的表达,并抑制缺血性损伤中的细胞凋亡。

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