深低温停循环（DHCA）术后神经系统功能障碍发生率高，但机制尚不明确。研究表明IGF-1/IGF1R通路在脑缺血缺氧性损伤过程中具有显著的保护作用，但目前尚未见该通路与DHCA相关的研究报道。课题组前期研究发现，DHCA术后大鼠海马组织中IGF1R表达显著升高，通过芯片筛查发现DHCA术后miRNA-223表达显著下调，而miRNA-223与IGF1R的调控密切相关，这可能是促进DHCA术后IGF1R表达上调的关键因素。本课题以IGF-1/IGF1R通路为核心，在体外培养神经元细胞及大鼠深低温停循环动物模型两个层面，通过慢病毒构建、海马立体定位注射等方法，分别上调和抑制IGF1R和miRNA-223的表达，从上游（miRNA-223）和下游（PI3K-Akt通路）两个方面，探索IGF-1/IGF1R 通路在DHCA脑保护的作用及其调控机制，为DHCA脑损伤的防治策略提供新的思路和方法。

Postoperative cerebral dysfunction is a common complication after DHCA (Deep hypothermic circulatory arrest) with a high incidence. The mechanisms have not yet been elucidated. A large number of studies have shown that IGF-1/IGF1R signaling pathway inhibites neuron apoptosis in cerebral anoxic injury process, showing cerebral protection effects. However, in the process of DHCA, there is little literature involved in this signaling pathway. Our preliminary research found that IGF1R expression increased significantly in hippocampus of rats on the third day after DHCA. Combined with chip screening and bioinformatics on website, the miRNA-223 is closely related to the regulation of IGF1R expression after DHCA. In this study, we plan to detect the IGF-1/IGF1R signal pathway on the basis of the cell and animal model, and explore the significance and regulatory mechanism of IGF-1/IGF1R signal pathway in the process of DHCA from the two aspects of upstream(miRNA-223) and downstream(PI3K-Akt). The study tries to provide a new thought and method about the research of brain protection after DHCA.