Abstract
Physical exercise has been shown to be beneficial in stroke patients and animal stroke models. However, the exact mechanisms underlying this effect are not yet very clear. The present study investigated whether pre-ischemic treadmill training could induce brain ischemic tolerance (BIT) by inhibiting the excessive glutamate release and event-related kinase 1/2 (ERK1/2) activation observed in rats exposed to middle cerebral artery occlusion (MCAO). Sprague–Dawley rats were divided into three groups (n = 12/group): sham surgery without prior exercise, MCAO without prior exercise and MCAO following three weeks of exercise. Pre-MCAO exercise significantly reduced brain infarct size (103.1 ± 6.7 mm3) relative to MCAO without prior exercise (175.9 ± 13.5 mm3). Similarly, pre-MCAO exercise significantly reduced neurological defects (1.83 ± 0.75) relative to MCAO without exercise (3.00 ± 0.63). As expected, MCAO increased levels of phospho-ERK1/2 (69 ± 5%) relative to sham surgery (40 ± 5%), and phospho-ERK1/2 levels were normalized in rats exposed to pre-ischemic treadmill training (52 ± 6%) relative to MCAO without exercise (69% ± 5%). Parallel effects were observed on striatal glutamate overflow. This study suggests that pre-ischemic treadmill training might induce neuroprotection by inhibiting the phospho-ERK1/2 over-activation and reducing excessive glutamate release
Highlights
This study suggests that pre-ischemic treadmill training might induce neuroprotection by inhibiting the phospho-eventrelated kinase 1/2 (ERK1/2) over-activation and reducing excessive glutamate release
Brain ischemic tolerance (BIT) is a phenomenon in which resistance to cerebral ischemia is induced by harmful stimuli that are below the threshold causing cell damage [1]
Phospho-ERK1/2 levels showed the same pattern as glutamate, but there was no effect on total ERK1/2. These results suggest that cerebral ischemia and exercise do not change ERK1/2 at the gene expression level, but pre-ischemic treadmill training can down-regulate the ischemia-induced increase of phospho-ERK1/2 and effectively protect the nervous system
Summary
Brain ischemic tolerance (BIT) is a phenomenon in which resistance to cerebral ischemia is induced by harmful stimuli that are below the threshold causing cell damage [1]. Several reports indicate that protective effects can be induced by normobaric hyperoxia [6], electro-acupuncture [7], and preischemic treadmill training [8], among others. During the past 20 years, the beneficial effects of physical exercise on stroke injury have been demonstrated, including reduction of neurologic deficits, amelioration of blood–brain barrier (BBB). A previous paper demonstrated that two or four weeks of treadmill pre-training was neuroprotective for ischemia, decreasing both cerebral infarction and edema [15]
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