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  • Title: Enriched Environment Enhances Poststroke Neurological Function Recovery on Rat: Involvement of p-ERK1/2.
    Author: Jiang C, Yu K, Wu Y, Xie H, Liu G, Wu J, Jia J, Kuang S.
    Journal: J Stroke Cerebrovasc Dis; 2016 Jul; 25(7):1590-1598. PubMed ID: 27068861.
    Abstract:
    BACKGROUND: Increasing evidence shows that exposure to an enriched environment (EE) after cerebral ischemia or reperfusion injury is neuroprotective in animal models, including that EE enhances functional recovery after ischemic stroke. However, the mechanism underlying this effect remains unclear. To clarify this critical issue, the current study investigated the effects of EE on the role of extracellular signal-regulated kinase (ERK) after cerebral ischemia or reperfusion injury of rat. METHODS: Adult rats were subjected to ischemia induced by middle cerebral artery occlusion (MCAO) followed by reperfusion. Ladder walking task and limb-use asymmetry task were used to test the recovery of rat behavior on postoperative days 1, 3, 5, 7, 14 and days 3, 7, 14, respectively. On the eighth day after MCAO, infarct volume was assessed by 2,3,5-triphenyltetrazolium chloride staining. Expressions of phosphorylated ERK1/2 (p-ERK1/2) and total ERK1/2 were examined by western blot, and electron microscopy was used to evaluate the astrocytes morphology surround in the perivascular 14 days after MCAO. RESULTS: EE improves the recovery of coordination and integration of motor movements on rats after cerebral ischemia or reperfusion injury. EE downregulates the level of p-ERK1/2 in the rat cortex after cerebral ischemia or reperfusion injury. Furthermore, EE reduces astrocytic swelling and injury. CONCLUSIONS: These findings suggest that EE could promote rehabilitation after ischemia via regulation of p-ERK1/2 expression, which may provide a therapeutic approach for cerebral ischemia or reperfusion injury. The suppression of postischemic astrocytic swelling in the brain of the ischemic rats through the intervention of EE would be one of the underlying mechanisms in the protective effect of cerebral ischemia.
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