缺血性脑卒中早期是脑功能重建极为敏感的时期,我们前期研究发现卒中后早期运动能增加脑血流灌注，激活血管内皮细胞胞膜上Tie-2受体介导的PI3K/AKT通路和Bcl-2通路，降低内皮细胞凋亡。但是血流诱导Tie-2激活的机制尚不清楚。既往观点认为胞膜受体无活性与磷脂双分子层脂筏的掩埋或亚基隔离有关，同时鞘磷脂酶（SMases）降解脂筏中的鞘磷脂(SM)可诱导脂筏重排，因此我们推测SMases对SM降解可能诱导了Tie-2胞膜蛋白激活。为验证这一假说，本课题拟通过研究卒中后早期运动训练引起的脑血流改变对大鼠缺血脑区SMases与Tie-2的影响，并在体外用适宜血流干预氧糖剥夺的内皮细胞，观察细胞水平上两者的变化，同时体内外研究均使用SMases抑制剂验证两者的相互作用，探索卒中后运动引起的血流改变是否通过脂筏重排，介导胞膜受体的激活，将力学信号转化为生物信号，达到降低脑损伤的作用。

Early period of ischemic stroke is the stage of brain functional reconstruction,exercise intervention in this time could improve the prognosis . Our previous study found that early exercise intervention after stroke increased the perfusion of ischemic brain regions to activate Tie-2 receptor on the endothelial cell membrane, The following activated PI3K/AKT pathway and Bcl-2 pathways reduced endothelial apoptosis and improved nerve function impairment.But Tie-2 activation mechanism is unclear.Scholars generally believe that no activity of the receptor on the cells membrane attributes to the buried isolation by the phospholipid bilayer, degradation of sphingomyelin in the lipid rafts by sphingomyelinase induces the rearrangement of lipid rafts. We hypothesize that the degradation of sphingomyelin may induce the activation of membrane protein Tie-2.To verify this hypothesis,we proposed to test the sphingomyelinase and Tie-2 on rats in vivo when the changes in cerebral blood flow caused by early training after stroke and on oxygen and glucose deprivated endothelial cells in vitro when using an appropriate intervention blood.We also observe the changes of both with the inhibitor of sphingomyelin. We aim to explore whether the changes in blood flow after early exercise training after stroke causes the lipid rafts rearrangement- mediated activation of membrane receptors to reduce brain injury.