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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >PRE-ISCHEMIC TREADMILL TRAINING ALLEVIATES BRAIN DAMAGE VIA GLT-1-MEDIATED SIGNAL PATHWAY AFTER ISCHEMIC STROKE IN RATS
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PRE-ISCHEMIC TREADMILL TRAINING ALLEVIATES BRAIN DAMAGE VIA GLT-1-MEDIATED SIGNAL PATHWAY AFTER ISCHEMIC STROKE IN RATS

机译：大鼠缺血性卒中后缺血前的跑步机训练小白菜通过GLT-1介导的信号通路对大脑的损害

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Physical exercise could play a neuroprotective role in both human and animals. However, the involved signal pathways underlying the neuroprotective effect are still not well established. This study was to investigate the possible signal pathways involved in the neuroprotection of pre-ischemic treadmill training after ischemic stroke. Seventy-two SD rats were randomly assigned into three groups (n = 24/group): sham surgery group, middle cerebral artery occlusion (MCAO) group and MCAO with exercise group. Following three weeks of treadmill training exercise, ischemic stroke was induced by occluding the middle cerebral artery (MCA) in rat for 2 h, followed by reper-fusion. Twenty-four hours after MCAO/reperfusion, 12 rats in each group were evaluated for neurological deficit scores and then sacrificed to measure the infarct volume (n = 6) and cerebral edema (n = 6). Six rats in each group were sacrificed to measure the expression level of glutamate transporter-1 (GLT-1), protein kinase C-alpha (PKC-alpha), Akt, and phosphatidylinositol 3 kinase (PI3K) (n = 6). Two hundred and eighty minutes (4.67 h) after occlusion, six rats in each group were decapitated to detect the mRNA expression level of metabotropic glutamate receptor 5 (mGluR5) and N-methyl-D-aspartate receptor subunit type 2B (NR2B) (n = 6).The results demonstrated that pre-ischemic treadmill training exercise reduced brain infarct volume, cerebral edema and neurological deficits, also decreased the over expression of PKC-alpha and increased the expression level of GLT-1, Akt and PI3K after ischemic stroke (p < 0.05). The over-expression of mGluRS and NR2B mRNA was also inhibited by pre-ischemic exercise (p < 0.05). In summary, exercise preconditioning ameliorated brain damage after ischemic stroke, which might be involved in two signal pathways: PKC-alpha-GLT-1-Glutamate and PI3K/Akt-GLT-1-Glutamate.
机译：体育锻炼可以对人和动物起到神经保护作用。然而，仍未很好地建立涉及神经保护作用的相关信号途径。本研究旨在探讨缺血性卒中后缺血前跑步机训练神经保护可能涉及的信号途径。将72只SD大鼠随机分为三组（每组24只）：假手术组，大脑中动脉闭塞（MCAO）组和运动组MCAO。经过三周的跑步机训练运动，通过阻塞大鼠大脑中动脉（MCA）2小时，然后再灌注，诱发了缺血性中风。 MCAO /再灌注后24小时，评估每组12只大鼠的神经功能缺损评分，然后处死以测量梗塞体积（n = 6）和脑水肿（n = 6）。处死每组六只大鼠以测量谷氨酸转运蛋白-1（GLT-1），蛋白激酶C-α（PKC-alpha），Akt和磷脂酰肌醇3激酶（PI3K）的表达水平（n = 6）。闭塞后280分钟（4.67小时），将每组六只大鼠断头以检测代谢型谷氨酸受体5（mGluR5）和N-甲基-D-天冬氨酸受体2B型（NR2B）的mRNA表达水平（n = 6）。结果表明，缺血前跑步机训练锻炼可减少脑梗死体积，脑水肿和神经功能缺损，还可以减少PKC-α的过表达并增加缺血性中风后GLT-1，Akt和PI3K的表达水平（p ＜0.05）。缺血前运动也抑制了mGluRS和NR2B mRNA的过表达（p <0.05）。总之，运动预处理可以减轻缺血性中风后的脑损伤，这可能与两个信号通路有关：PKC-α-GLT-1-谷氨酸和PI3K / Akt-GLT-1-谷氨酸。

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