局灶性脑缺血大鼠纹状体区域Shh信号通路成分的表达变化及对髓鞘修复的影响  

The expression changes of Sonic Hedgehog signaling pathway in the striatum after focal cerebral ischemia in rats and its role on remyelination

作　　者：赵红[1] 吴晓君[2] 刘赞华[1] 王苏平[1] 闫旭[2] 

机构地区：[1]大连市中心医院神经内科,大连辽宁116033 [2]大连医科大学,在读研究生大连辽宁116044

出　　处：《中风与神经疾病杂志》2016年第7期629-632,共4页Journal of Apoplexy and Nervous Diseases

摘　　要：目的检测Sonic Hedgehog(Shh)信号通路及其转录因子Gli1在局灶性脑缺血后不同时间点的表达变化,探讨该通路对脑缺血后髓鞘再生的影响。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RT-PCR的方法观察脑缺血后1 d,3 d,7 d和14 d Shh,Gli1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,观察脑缺血后上述各时间点MBP的表达变化。结果正常大鼠Shh和Gli1广泛分布于脑白质和灰质,如皮质,胼胝体和纹状体等区域。Shh和Gli1的表达在脑缺血后3 d^14 d呈逐渐上升趋势。MBP的表达在脑缺血后1 d^28 d逐渐下降。结论脑缺血性损伤可激活Shh信号通路,激活的Shh可能通过调控细胞的增殖参与神经修复,针对Shh的表达量进行干预治疗将为脱髓鞘疾病的治疗提供理论依据。Objective Sonic Hedgehog（Shh） signal pathway regulates precursor cells proliferation and differentiation and is involved in the neurogenesis after ischemia.Our study is to explore the expression changes of Shh and its transcription factor Gli1 at different time points after focal cerebral ischemia and the effect of Shh on myelin repair.Methods We used the middle cerebral artery occlusion（MCAO） for 120 min as a rat model.MBP was used as a marker of myelin.Used immunohistochemistry and RT-PCR technique,we detected the expression of Shh,Gli1 and MBP at different time points after focal cerebral ischemia.Results Shh and Gli1 were distributed throughout the white and gray matter of the normal brain,such as cortex（Cx）,corpus callosum（cc） and striatum（Str）.In addition,Shh and Gli1 expression significantly increased from day 3 to day 14 after MCAO.The expression of MBP gradually reduced from day 1 to day 14 in MCAO rats.Conclusion The ischemia injury can activate Shh signal pathway.The activation of Shh might promote remyelination through regulating the neural precursor cells proliferation,which might have implications in the treatment of demyelinating disease.

关 键 词：局灶性脑缺血 SHH信号通路 GLI1 髓鞘再生 

分 类 号：R743.3[医药卫生—神经病学与精神病学]