中文摘要：

目的探讨Olig1在局灶性脑缺血后不同时间点的表达变化及其参与髓鞘修复的可能机制。方法线栓法建立大脑中动脉闭塞（middle cerebral artery occlusion,MCAO）模型,使用免疫组化和Western blot的方法观察脑缺血后1d、3d、7d、14d和28d Olig1的表达变化。碱性髓鞘蛋白（myelin basic protein,MBP）是髓鞘的组成成分,用作髓鞘的标志物,检测脑缺血后上述各时间点MBP的表达变化。结果正常大鼠Olig1广泛分布于脑白质和灰质,如皮层、胼胝体和纹状体等区域,典型地沿着神经纤维成束状排列。正常大鼠Olig1主要位于少突胶质细胞的胞浆,脑缺血后Olig1由胞浆移至细胞核。Olig1的表达在脑缺血后1d下降,3d回到正常水平并维持此水平到脑缺血后28d。MBP蛋白表达在脑缺血后1d至28d逐渐下降。结论 Olig1在脑缺血的初期表达下降,抑制了神经的再生,针对Olig1的表达规律进行干预将为脑缺血后髓鞘的修复提供理论依据。

英文摘要：

Objective Transcription factor Olig1 plays an important role in demyelinated lesions repairment,and our study is to investigate the expression pattern of Olig1 after focal cerebral ischemia and its role in remyelination.Methods Myelin basic protein（MBP） was used as a marker of myelin.Transient focal ischemia was induced by middle cerebral artery occlusion（MCAO） for 120 minutes with a nylon filament.Immunohistochemical and Western Blot technique were used,and Olig1 and MBP were detected at different time points after focal cerebral ischemia.Results Olig1 was expressed in the cytoplasm of oligodendrocytes and distributed throughout the white and gray matter of the normal brain,such as cortex（Cx）,corpus callosum（cc） and striatum（Str）.When the brain underwent ischemia,Olig1 translocated from cytoplasm into nucleus.In addition,olig1 expression significantly decreased on 1d after MCAO,then returned to the normal level from 3d to 28d.MBP gradually reduced from 1d to 28d in MCAO rats.Conclusion The decrease of Olig1 in the initial 24h after ischemia might inhibit myelin repair,which might have implications in neural regeneration.