Ischemic postconditioning enhances glycogen synthase kinase-3β expression and alleviates cerebral is

来源 :Neural Regeneration Research | 被引量 : 0次 | 上传用户:wy19841010
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The present study established global brain ischemia using the four-vessel occlusion method.Following three rounds of reperfusion for 30 seconds,and occlusion for 10 seconds,followed by reperfusion for 48 hours,infarct area,the number of TUNEL-positive cells and Bcl-2 expression were significantly reduced.However,glycogen synthase kinase-3β activity,cortical Bax and caspase-3 expression significantly increased,similar to results following ischemic postconditioning.Our results indicated that ischemic postconditioning may enhance glycogen synthase kinase-3β activity,a downstream molecule of the phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B signaling pathway,which reduces caspase-3 expression to protect the brain against ischemic injury. The present study established global brain ischemia using the four-vessel occlusion method. Two rounds of reperfusion for 30 seconds, and occlusion for 10 seconds followed by reperfusion for 48 hours, infarct area, the number of TUNEL-positive cells and Bcl- 2 expressions were significantly reduced. However, glycogen synthase kinase-3β activity, cortical Bax and caspase-3 expression were significantly increased, similar to results following ischemic postconditioning. Our results indicated that ischemic postconditioning may enhance glycogen synthase kinase-3β activity, a downstream molecule of the phosphatase and tensin homolog deleted on chromosome 10 / phosphatidylinositol 3-kinase / protein kinase B signaling pathway, which reduces caspase-3 expression to protect the brain against ischemic injury.
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