Early Exercise Protects against Cerebral Ischemic Injury through Inhibiting Neuron Apoptosis in Cortex in Rats

Abstract

Early exercise is an effective strategy for stroke treatment, but the underlying mechanism remains poorly understood. Apoptosis plays a critical role after stroke. However, it is unclear whether early exercise inhibits apoptosis after stroke. The present study investigated the effect of early exercise on apoptosis induced by ischemia. Adult SD rats were subjected to transient focal cerebral ischemia by middle cerebral artery occlusion model (MCAO) and were randomly divided into early exercise group, non-exercise group and sham group. Early exercise group received forced treadmill training initiated at 24 h after operation. Fourteen days later, the cell apoptosis were detected by TdT-mediated dUTP-biotin nick-end labeling (TUNEL) and Fluoro-Jade-B staining (F-J-B). Caspase-3, cleaved caspase-3 and Bcl-2 were determined by western blotting. Cerebral infarct volume and motor function were evaluated by cresyl violet staining and foot fault test respectively. The results showed that early exercise decreased the number of apoptotic cells (118.74 ± 6.15 vs. 169.65 ± 8.47, p < 0.05, n = 5), inhibited the expression of caspase-3 and cleaved caspase-3 (p < 0.05, n = 5), and increased the expression of Bcl-2 (p < 0.05, n = 5). These data were consistent with reduced infarct volume and improved motor function. These results suggested that early exercise could provide neuroprotection through inhibiting neuron apoptosis.

Maternal hypoxia increases hippocampal cell susceptibility to ischemia after middle cerebral artery occlusion in rat offspring

“…Apoptosis is one of the major cell death patterns in this ischemic penumbra [4]. Consistent with a previous finding [20], our results demonstrated that MCAO contributed to cell apoptosis in the ipsilateral hippocampal region following ischemia. Furthermore, our data also showed that maternal hypoxia did not directly lead to obvious hippocampal cell apoptosis, but it exacerbated brain cell damage and intensified apoptosis in the hippocampus of rat offspring exposed to cerebral ischemia.…”

“…Previous studies have demonstrated that caspase-3 expression increases after stroke [20]. Deletion or inhibition of caspase-3 induces neuroprotective effects via a reduction in cerebral infarct size and prolongs the therapeutic window [6,13,20]. In the present study, we demonstrated that MCAO increased the levels of caspase-3 and cytochrome c in the rat hippocampus.…”

“…Thus, we measured caspase-3 and cytochrome c expression in the hippocampus ipsilateral to ischemia. Previous studies have demonstrated that caspase-3 expression increases after stroke [20]. Deletion or inhibition of caspase-3 induces neuroprotective effects via a reduction in cerebral infarct size and prolongs the therapeutic window [6,13,20].…”

Treadmill exercise promotes neuroprotection against cerebral ischemia&ndash;reperfusion injury via downregulation of pro-inflammatory mediators

“…However, a growing number of studies have shown that exercise is an effective rehabilitation program for improving clinical outcomes of stroke 6,7. Beneficial effects of exercise in stroke patients are also supported by studies in animal models through attenuating pro-inflammatory reactions or inhibiting neuron apoptosis 8,9…”

Physiological Adaptations Following Endurance Exercises after Stroke: Focus on the Plausible Role of High-Intensity Interval Training

“…Indeed, several authors indicated that endurance training reduced infarct volume during the first weeks after cerebral ischemia [28][29][30][31]. Moreover, an early and daily treadmill exercise during 1 month increased the cellular expression levels of some neurotrophic factors, promoted cell growth and neural plasticity, but also reduced the expression of apoptosis markers [28, 31,32].…”