Objective To observe the effect of treadmill exercise on the expression of transforming growth factor-β1 (TGF-β1) and its receptor Smad3 protein as well as on cell apoptosis in the ischemic boundary zone,so as to explore how exercise promotes the recovery of neurological function after cerebral ischemia.Methods Thirty adult male Sprague-Dawley rats were randomly divided into a sham group (n=6),a model group (n=12) and an exercise group (n=12).A modified Longa's method was used to establish an animal model of cerebral ischemia by occluding the right middle cerebral artery in the rats of the model and exercise groups.Those of the sham group were subjected to the same surgical procedure except that no thread was inserted.After 24h the exercise group began treadmill training,while the other two groups were left on the treadmill without training.Modified neurological severity scores (mNSSs) were used to quantify the rats' neurological functioning on the 3rd,7th and 14th day after the surgery.The ischemic boundary zone tissue was then dissected to detect the expression of TGF-31 and Smad3 protein using western blotting.Cell apoptosis was detected by TUNEL staining.Results The average mNSS scores of the exercise group on the 7th and the 14th day were significantly lower than those of the model group at the same time points.The average expression level of TGF-β1 and Smad3 protein in the exercise group was significantly higher than in the model group.The number of TUNEL-positive cells in the exercise group was significantly lower than in the model group on the 14th day.Conclusions Treadmill exercise can improve the recovery of neurological function after cerebral ischemia.It may be partly due to upregulating the expression of TGF-β1 and Smad3 protein,which inhibit cell apoptosis in the ischemic boundary zone.

Objective:To study the effect of rehabilitation training on the expression of neuroglobin (Ngb), oxidative stress and axon regeneration in the cortex and explore possible mechanisms of functional recovery after cerebral infarction.Methods:Thirty-six male Sprague-Dawley rats were randomly divided into a sham operation group, a model group and a rehabilitation group. Cerebral infarction was modelled in the model and rehabilitation groups using Longa′s middle cerebral artery occlusion (MCAO) technique. The sham operation group received the same procedure except that no thread was inserted to block the middle cerebral artery. The rats in the rehabilitation group began treadmill training 24h after the operation, while the other two groups were left on the treadmill without training. On the 3rd, 7th and 14th days after the operation, all of the rats′ neurological functioning was assessed using modified neurological severity scores (mNSSs). After the last mNSS test, all of the rats were sacrificed and peri-infarct brain tissue was resected to detect the expression of Ngb and oxidative stress indicators including superoxide dismutase (SOD), nitric oxide and malondialdehyde (MDA), as well as neurofilament-200 (NF-200) indicating axon regeneration.Results:On the 3rd day after the surgery there was no significant difference between the average mNSS scores of the rehabilitation and model groups. On the 7th and 14th day the average mNSS score of the rehabilitation group was significantly better than that of the model group. The average expression of Ngb in the model group was significantly higher than in the sham operation group. After the intervention, the average expression of SOD in the rehabilitation group was significantly higher than in the model group, while NO and MDA expression were significantly lower. After the intervention the average expression of NF-200 in the rehabilitation group was also significantly higher than in the model group.Conclusions:Rehabilitation training benefits the recovery of neurological function after cerebral infarction, at least in rats. The mechanism may be related to the upregulation of Ngb, alleviation of oxidative stress and enhancement of axonal regeneration in the peri-infarct cortex.