The Study Glial Regeneration and Neuroprotection on Brain Ischemic Model

众所周知，大脑中动脉(MCA)闭塞会导致大脑中动脉(MCA)区域发生脑梗塞，继而导致大脑中动脉区域神经元丢失和胶质细胞改变。α-突触核蛋白是一种突触前蛋白，在帕金森病和突触小体疾病中明显存在于路易小体中。我们检测了神经退行性损伤后α-突触核蛋白的变化，并与MAP2(神经元标记物)、CD11b(小胶质细胞标记物)、GFAP(星形胶质细胞标记物)和HO-1(应激标记物)进行了比较。大脑中动脉结扎再灌流2小时后，同侧纹状体和大脑皮质MAP2免疫反应在1天后明显消失。而α-突触核蛋白的免疫反应性在大脑中动脉结扎后3天和7天仍无明显变化，与KA注射后相似。在大脑皮层和纹状体MAP2免疫反应缺失的区域(梗死灶)可见大量CD11b免疫阳性的小胶质细胞，而在边缘区(病灶周围)可见GFAP免疫阳性的星形胶质细胞被激活。此外，MCA结扎后可见大量MAP2免疫阳性的胶质样细胞，提示激活的胶质细胞可诱导变性神经元的吞噬作用。因此，α-突触核蛋白可能不会被神经胶质细胞清除，尽管许多神经元和树突因神经退行性损伤而丢失。因此，α-突触核蛋白很容易凝聚在神经退行性变的区域。

It is known that occlusion of the middle cerebral artery (MCA) induces infarction and then neuronal loss and glial changes in the territory region of the MCA. α-Synuclein, a presynaptic protein, is markedly included in Lewy bodies (LB) in Parkinson's and LB diseases. We examined changes of α-synuclein after neurodegenerative insults such as MCA occlusion and KA injection, in comparison with MAP2 (a neuronal marker), CD11b (a microglial marker), GFAP (an astroglial marker) and HO-1 (a stress marker). After 2-h MCA occlusion and reperfusion, MAP2-immunoreactivity was markedly lost in the ipsilateral side of the striatum and cerebral cortex after 1 day. However, the immunoreactivities of α-synuclein did not markedly change even at 3 and 7 days after MCA occlusion, similar to after KA injection. Numerous CD11b-immunopositive microglia were observed in the regions (infarcted core) where MAP2 immunoreactivity was lost in the cerebral cortex and striatum, while GFAP-immunopositive astrocytes were activated in the border zones (perifocal regions). In addition, numerous MAP2-immunopositive glia-like cells were observed after MCA occlusion, suggesting that activated glial cells induced the phagocytosis of degenerating neurons. Thus, α-synuclein protein might not be scavenged by glial cells, although numerous neurons and dendrites are lost by neurodegenerative insults. Therefore, α-synuclein protein may readily condense in neurodegenerative regions.