早产儿脑损伤的修复机制尚不明确，致使其治疗无突破性进展。我们前期芯片研究发现，缺氧缺血未成熟大鼠脑组织miR-200b表达明显下调，在培养脑片中敲低miR-200b，Rac1和Slit2表达均明显提高，但miR-200b对缺氧缺血性脑损伤结局的影响及其机制尚不明确。本研究拟将miR-200b及反向序列转染至未成熟大鼠缺氧缺血脑组织，通过神经行为评估等了解其对缺氧缺血结局的影响；利用示踪技术分析miR-200b对少突胶质细胞增殖及轴突再生的影响,电镜检测形态学变化，能量代谢水平检测线粒体活性。然后在离体水平用荧光素酶报告系统检验miR-200b对Rac1及Slit2的靶向调节作用，分析少突胶质细胞增殖、迁移情况及轴突生长的变化,进而揭示其对髓鞘以及轴突影响的具体机制；以检验"mir-200b是否通过Rac1和Slit2调节未成熟新生大鼠缺氧缺血脑损伤髓鞘修复和轴突导向"，为治疗提供实验依据。

The treatment of brain damage in preterm infant has no breakthrough because of the repairment mechanism still unclear. Our previous chip studies found the expression of miR-200b was significantly decreased in hypoxic-ischemic premature rat brain,however,the expression of Rac1 and Slit2 were significantly increased when knockdown miR-200b in cultured brain slice. The effection of miR-200b on hypoxia/ischemia brain damage(HIBD) and regulation mechanism remain unknown,therefore, we plan to transfect miR-200b and reverse sequence to hypoxic-ischemic premature rat brain, analyze the influence on hypoxia/ischemia through neurobehavioral evaluation, the effection of miR-200b on oligodendrocyte proliferation and axon regeneration by tracer technique, morphologic variations by electron microscope, mitochondria activity from metabolic level.Then detect the regulation of miR-200b on Rac1 and Slit2 by luciferase reporter system in vitro, observe the proliferation, migration of oligodendrocyte and axon growth, try to explain the role of miR-200b on myelin sheath and axon, confirm whether miR-200b regulating myelin sheath repairment and axon guidance through Rac1 and Slit2 in premature rat with HIBD, provide scientific basis for treatment.