Background and objectives: Stroke is one of the leading causes of death and long-term acquired disability. It is of great importance to seek ways for improving motor, sensory, and cognitive function after stroke and brain injury. In this regard, therapeutic exercise is the most commonly used method of rehabilitation that can significantly reduce the severity of functional damage. The aim of the present study was to investigate effects of eight weeks of forced treadmill training on cognitive and motor functions in ischemic rats.Methods: Fourteen adult male Wistar rats were divided into an exercise group and a control group (no exercise). Occlusion of both common carotid arteries was made to induce cerebral ischemia. Twenty-four hours after the induction of ischemia, the subjects in the exercise group were subjected to treadmill running, five days a week for eight weeks. The skilled ladder rung walking task was used to evaluate motor function before and after the stroke.Results: The number of errors was decreasing in both groups, but significant differences were observed in the motor function between the two groups in the third, fifth, and eighth week.Conclusion: Our results suggest that post-ischemic exercise might modulate ischemia-induced hippocampal injury and ameliorate the subsequent memory and motor impairment.
Introduction: Although exercise is an effective strategy for preventing and treating stroke, the extent of this effect seems to depend on when exercise begins. Apoptosis plays a critical role after stroke. However, it is unclear whether early exercise inhibits apoptosis after stroke? The aim of this study was to determine the effect of eight weeks of early aerobic training after stroke induction on caspase-3 protein expression and apoptosis in the hippocampus of male Wistar rats.
Methods: In this experimental study, 32 adult male Wistar rats (weighting 210-252 gr) were purchased and randomly divided into four groups: sham, ischemia, training and ischemia+ training groups. Ischemia was induced by the occlusion of both common carotid arteries (CCA) for 45 min. Aerobic training was initiated at 24 hours after induction of ischemia, for eight weeks for 20-50 minutes and at a speed of 18-30 meters per minute in each session and five sessions per week. Forty eight hours after the last training session, rats were sacrificed, then using immunohistochemical staining technique of caspase-3 protein expression and the rate of cell apoptosis were measured by hematoxylin and eosinophil (H&E) staining method in hippocampus of rats.
Results: The expression of caspase-3 protein and apoptosis in the hippocampus of rats in sham and training groups were significantly lower than in the ischemia and ischemia+ training groups (both; p<0.0001). Moreover, in the ischemia+ training group, the expression of caspase-3 protein and apoptosis showed a significant decrease compared to the ischemia group (p<0.0001).
Conclusion: Based on the results of this study, it can be said that eight weeks of early aerobic training can reduce the lesions induced-cerebral ischemia by reducing the expression of cell death-causing factors.
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