Wang Q, Wang P-P, Meng P-P, Han C, Yue S-W
Department of Physical Medicine & Rehabilitation, Qilu Hospital, Medical School of Shandong University, Jinan, China.
Eur Rev Med Pharmacol Sci. 2016 Sep;20(18):3839-3852.
Cerebral ischemia-reperfusion is the major pathophysiological process in stroke and can cause severe and lasting sequel. However, an intensive exercise training can potentially effect a quick and efficient recovery. We used swimming training on rats with cerebral ischemia-reperfusion (CIR) and explore the underlying neuroprotective mechanism(s), including the effects of intensive training on the expression of semaphorin 3A (Sema3A) and its receptor Neuropilin-1 (NRP-1).
The middle cerebral artery occlusion/reperfusion (MCAO/R) model was established by inserting a thread into the middle cerebral artery of Sprague-Dawley (SD) rats, and randomly dividing into the control group and training groups for different training intensities. The control group and the sham group received no training. All the rats in various groups were further randomly divided into three sub-groups for different postoperative time points (3, 7, and 14 days after operation). The apoptosis and the expression of Sema3A and NRP-1 were analyzed using immunohistochemistry (IHC), RT-PCR, and Western blotting methods respectively.
The intensive training resulted in significant neurological function improvements at all the time points after MCAO, compared to that in the control group (p<0.05), with training group 3 (highest training intensity) showing the most remarkable recovery. The Sema3A and NP-1 expressions were significantly lower than those of the control group at all the time points (p<0.05), with training group 3 having the lowest levels (best recovery).
Intensive training can reduce cerebral damage after ischemia and reperfusion in rats, inhibit the MCAO-induced Sema3A and NRP-1 expression, and accelerate the restoring process of motor nerve functions.
脑缺血再灌注是中风的主要病理生理过程，可导致严重且持久的后遗症。然而，高强度运动训练可能会实现快速有效的恢复。我们对脑缺血再灌注（CIR）大鼠进行游泳训练，并探究其潜在的神经保护机制，包括高强度训练对信号素3A（Sema3A）及其受体神经纤毛蛋白-1（NRP-1）表达的影响。
将线插入Sprague-Dawley（SD）大鼠大脑中动脉，建立大脑中动脉闭塞/再灌注（MCAO/R）模型，并随机分为对照组和不同训练强度的训练组。对照组和假手术组不接受训练。各实验组的所有大鼠进一步随机分为三个亚组，用于不同的术后时间点（术后3、7和14天）。分别采用免疫组化（IHC）、逆转录-聚合酶链反应（RT-PCR）和蛋白质免疫印迹法分析细胞凋亡以及Sema3A和NRP-1的表达。
与对照组相比，高强度训练使MCAO术后各时间点的神经功能均有显著改善（p<0.05），训练组3（训练强度最高）恢复最为显著。各时间点Sema3A和NP-1的表达均显著低于对照组（p<0.05），训练组3的水平最低（恢复最佳）。
高强度训练可减轻大鼠缺血再灌注后的脑损伤，抑制MCAO诱导的Sema3A和NRP-1表达，并加速运动神经功能的恢复过程。
