脑卒中是老年人常见、多发病之一，具有极高的致死率和致残率。外泌体作为胞间信息传递介质，在脑卒中等复杂中枢神经系统疾病的研究中具有巨大优势和研究价值。前期通过外泌体基因芯片分析发现Zeb2和Axin2在缺血性脑卒中后表达上调，可能参与脑卒中后脑组织的神经修复过程。为了进一步探究Zeb2/Axin2的作用机制，本项目拟创建大鼠脑缺血再灌注模型，研究外泌体Zeb2/Axin2对缺血性脑卒中的神经保护机制，同时通过氧糖剥夺体外模型，探究富含Zeb2/Axin2大鼠BMSCs及其外泌体对少突胶质细胞祖细胞（OPCs）凋亡、增殖、分化，迁移的影响及其分子机制，并进一步探究分析Zeb2和Axin2之间的相互作用关系。本研究利用外泌体芯片技术筛选出外泌体介导的神经保护基因Zeb2/Axin2，并探究其对缺血性脑卒中的脑保护分子机制，其研究成果将有助于缺血性脑卒中的神经功能保护，并为治疗提供新的思路。

stroke is one of the common disease and frequently-occurring disease in the elderly, which has a very high mortality and morbidity. Exosomes as intercellular information transfer media, have great potential advantage and research value in the study of complex diseases of the central nervous system. The study found that Zeb2 and Axin2 expression were upregulated after ischemic stroke by exosomes gene chip analysis, which may participate in brain nerve repair process of the organization after ischemic stroke. In order to further explore the mechanism of action of Zeb2/Axin2, this research intends to explore exosomes contain Zeb2/Axin2 for nerve protective mechanisms after ischemic stroke through creating ischemia-reperfusion rats model by the middle cerebral artery occlusion (MCAO). In vitro, OGD model was used to explore the effect of enriched BMSCs and exosomes of Zeb2/Axin2 on oligodendrocytes progenitor cells (OPCs) proliferation, differentiation, migration, myelin regeneration and its molecular mechanism, moreover, the relationship between Axin2 and Zeb2 was also explored and analysed. This study points out that the cerebral protective mechanisms of the enriched exosomes of Zeb2/Axin2 after ischemic stroke for the first time, and the research results will help to repair brain nerve after ischemic stroke, and provide new ideas for the treatment of ischemic stroke.