脑缺血性损伤之后继发的神经炎症反应是影响神经功能修复、导致不良预后的关键病理机制。间充质干细胞外泌体（MSCs-exosomes）治疗脑缺血损伤具有良好的转化前景，但调控神经炎症作用薄弱，目前尚无优化的干预方案和疗效机制。反应性星形细胞（RA）A1/A2表型调控是干预神经炎症反应的新途径。芎归药对治疗缺血性中风临床基础良好，课题组前期研究发现芎归方具有促进神经修复、调节炎症微环境的作用。本项目拟结合前期时间差异蛋白组学及生信分析结果，以miR-30e/CaN-NFAT与NF-κB/PI3K-Akt通路串话调控RA表型为研究主线，探讨芎归方协同MSCs-exosomes干预脑缺血损伤神经炎症反应的作用机制，为临床转化提供依据。

The neuroinflammatory response after cerebral ischemic injury is a key pathological mechanism that affects neurological repair and leads to poor prognosis. Mesenchymal stem cell exosomes (MSCs-exosomes) have a positive transformation prospect in the treatment of cerebral ischemic injury, but the regulation of neuroinflammation is limited. There has been no optimized intervention and efficacy mechanism for now. Reactive astrocyte (RA) A1/A2 phenotypic regulation is an innovative approach for the neuroinflammatory response intervention. The combination of Chuanxiong and Danggui is effective on treatment for ischemic stroke in clinic. Our research group found that Xionggui formula has the function of promoting nerve repair and regulating the inflammatory microenvironment in the previous study. This research intends to combine the temproal differential proteomics and Bioinformatics analysis results of our previous study focuses on regulation of RA phenotype by miR-30e/CaN-NFAT and NF-κB/PI3K-Akt pathway crosstalk to discuss Xionggui formula combined with MSCs-exosomes for the intervention and mechanism in the neuroinflammatory response after cerebral ischemic injury, which may provide a basis for further clinical transformation.