脑缺血激活的神经轴突再生、神经祖细胞(NPCs)增殖迁移及分化等内源性修复机制对卒中后神经功能的恢复至关重要，但由于中枢神经系统再生能力弱，加之缺血后反应性星形胶质细胞(RAs) 形成的胶质瘢痕(GS)会抑制轴突再生能力、限制梗死区周围皮质(PIC)的再生微环境，导致神经自我修复能力不足。RAs具有干细胞特性，在外因作用下可被重编程为神经元。促使GS内RAs重编程为神经元不仅可减轻对轴突再生的抑㓡、改善PIC再生微环境，还可协同NPCs补偿梗死区损失的神经元，是促进内源性神经修复机制的关键环节。课题组前期研究证实天麻4#酚性成分可改善脑缺血大鼠神经功能、增加PIC内Nestin+及NeuN+细胞数；体外实验显示其具有将RAs重编程为神经元的作用。本课题拟从介导GS内RAs重编程为神经元的角度，研究天麻4#酚性成分促进脑缺血后神经修复的作用，并阐明其作用机制。

Endogenous neurorepair is activated following cerebral ischemia, which intents to restore neurofunction through axonal regeneration of impaired neurons, as well as migration and differentiation of neural progenitor cells. However, due to the very limited ability of the neurorepair in central nervous system and the glial scar formed by reactive astrocytes (RAs) after ischemia, the self-repairing mechanism is too far to promote the recovery of neurofunction. RAs have the characteristics of neural stem cells. Under the exogenous factors such as transcription factors and small molecule compounds，RAs can be reprogrammed into neurons. Reprogramming of RAs in the glial scar into neurons not only reduce the inhibitory effect on axonal regeneration, but also provide a new source of neurogenesis, which is an important way to promote endogenous repair mechanisms. In our previous study, we have demonstrated that phenolic compound 4# of Gastrodia elata. can improve the neurological function of rats undergo cerebral ischemic and increase the positive expression of Nestin, a marker of neuronal stem cells, and NeuN, a marker of neurons in the peri-infarction cortex. In vitro experiments show that compound 4# can reprogram RAs into neurons, suggesting that it may plays a pivotal role in promoting nerurorepair. Based on the previous work, this project aims to explore the effect of 4# on neurorepair via reprogramming RAs into neurons, and to elucidate the related mechanisms.