【摘 要】
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Background It is well known that physical exercise is beneficial to functional recovery after stroke,but the mechanisms are poorly understood.Transient focal cerebral ischemia induces autophagy,apopto
【机 构】
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Department of Rehabilitation Medicine,the Third Affiliated Hospital,Sun Yat-sen University,Guangzhou
【出 处】
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第四届粤港澳台物理医学与康复学学术会议暨2013年广东省医学会物理医学与康复学学术会议
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Background It is well known that physical exercise is beneficial to functional recovery after stroke,but the mechanisms are poorly understood.Transient focal cerebral ischemia induces autophagy,apoptosis and neurogenesis in the peri-infarct region,all of which are related with the recovery of damaged brain.This study is aimed to examine the effect of physical exercise on autophagy,apoptosis and neurogenesis in the peri-infarct region in rat model of transient middle cerebral artery occlusion (MCAO).Results We found that autophagy marker microtubule-associated protein 1A light chain 3-II (LC3-II) was increased following cerebral ischemia,and physical exercise markedly reduced the expression of LC3-II in the peri-infarct region.The number of TUNEL-positive (deoxynucleotidyl transferase-mediated dUTP in situ nick-end labeling,an apoptosis marker) cells decreased,while Ki67-positive (a proliferative marker) and insulin-like growth factor-1 (IGF-1) increased more quickly in physical exercise group in comparison with that in control group after ischemia.Furthermore,LC3-punctates co-located with TUNEL-positive cells in the peri-infarct region.Conclusions The present data demonstrates that physical exercise enhances neurological function possibly by reducing autophagosomes accumulation,mitigating apoptosis as well as promoting neurogenesis in the peri-infarct region after transient cerebral infarction in rats.
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