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首页> 外文期刊>Journal of Neurochemistry: Offical Journal of the International Society for Neurochemistry >Neuroprotective effect of exercise in rat hippocampal slices submitted to in vitro ischemia is promoted by decrease of glutamate release and pro-apoptotic markers
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Neuroprotective effect of exercise in rat hippocampal slices submitted to in vitro ischemia is promoted by decrease of glutamate release and pro-apoptotic markers

机译:谷氨酸释放和促凋亡标记物的减少可增强运动对大鼠体外缺血海马切片的神经保护作用

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摘要

The role of physical exercise as a neuroprotective agent against ischemic injury has been extensively discussed. Nevertheless, the mechanisms underlying the effects of physical exercise on cerebral ischemia remain poorly understood. Here, we investigate the hypothesis that physical exercise increases ischemic tolerance by decreasing the induction of cellular apoptosis and glutamate release. Rats (n=50) were submitted to a swimming exercise protocol for 8weeks. Hippocampal slices were then submitted to oxygen and glucose deprivation. Cellular viability, pro-apoptotic markers (Caspase 8, Caspase 9, Caspase 3, and apoptosis-inducing factor), and glutamate release were analyzed. The percentage of cell death, the amount of glutamate release, and the expression of the apoptotic markers were all decreased in the exercise group when compared to the sedentary group after oxygen and glucose deprivation. Our results suggest that physical exercise protects hippocampal slices from the effects of oxygen and glucose deprivation, probably by a mechanism involving both the decrease of glutamatergic excitotoxicity and apoptosis induction.
机译:体育锻炼作为抗缺血性损伤的神经保护剂的作用已得到广泛讨论。然而,体育锻炼对脑缺血的潜在机制仍然知之甚少。在这里,我们调查体育锻炼通过减少诱导细胞凋亡和谷氨酸释放增加缺血耐受性的假设。大鼠(n = 50)进行了8周的游泳锻炼方案。然后将海马切片剥夺氧气和葡萄糖。分析细胞活力,促凋亡标记物(胱天蛋白酶8,胱天蛋白酶9,胱天蛋白酶3和凋亡诱导因子)和谷氨酸释放。缺氧和缺糖后,运动组与久坐组相比,细胞死亡百分比,谷氨酸释放量和凋亡标志物的表达均降低。我们的结果表明,体育锻炼可能通过涉及降低谷氨酸能兴奋性毒性和诱导细胞凋亡的机制来保护海马片免受氧和葡萄糖剥夺的影响。

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