Intensive training accelerates the recovery of motor functions following cerebral ischemia-reperfusion in MCAO rats

Q. Wang, P.-P. Wang, P.-P. Meng, C. Han, S.-W. Yue

Department of Physical Medicine & Rehabilitation, Qilu Hospital, Medical School of Shandong University, Jinan, China. shouweiy@sdu.edu.cn

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• Neurology

OBJECTIVE: 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).

MATERIALS AND METHODS: 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.

RESULTS: 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).

CONCLUSIONS: 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.

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