围术期脑缺血是严重影响手术患者预后的并发症，而高血糖作为围术期常见现象，可直接导致或加重脑缺血损伤。目前认为星形胶质细胞（As）功能在脑缺血损伤中扮演重要角色，As激活后可分为A1损伤型和A2修复型，但其参与脑缺血损伤的作用和机制不明。我们前期研究发现高血糖可诱导脑缺血后As向A1型转化，且这一过程与Cx43（缝隙连接蛋白43）-Nrf2通路的调控相关。由此推断：Cx43-Nrf2通路介导A1型转化导致高血糖条件下的脑缺血损伤加重，调控Cx43表达可使其改善。我们将通过体内、体外模型，采用RNA干扰、质粒转染等手段，旨在探讨：①As表型转化与脑缺血后神经炎性反应的相关性；②高血糖条件下Cx43-Nrf2通路对As表型转化的调控；③干预Cx43-Nrf2通路对As表型转化及脑缺血损伤的影响。本研究将从As表型转化这个新视角揭示高血糖致脑缺血损伤的分子机制，并为围术期脑缺血的防治提供新思路。

Perioperative cerebral ischemia is a serious complication in surgical patients and a critical problem needed to be solved. Hyperglycemia, as a common phenomenon in perioperative period, could induce or aggravate cerebral ischemia injury. Recent views suggest astrocyte play a critical role in cerebral ischemia injury, while the related mechanism remained unclear. Our previous investigation indicated that hyperglycemia could transfer astrocyte from protective type A2 to destructive type A1 under cerebral ischemia, possibly via Cx43-Nrf2 pathway. Therefore, we hypothesized that the phenotypic transformation of astrocyte modulated by Cx43-Nrf2 pathway induced an aggravating injury after cerebral ischemia under hyperglycemia, and the regulation of Cx43 could alleviate the damage. To test this hypothesis, we’ll testify the correlation between the phenotype transformation of astrocyte and neuroinflammation under cerebral ischemia, and we’ll also determine the possible new regulatory mechanism of Cx43-Nrf2 pathway on hyperglycemia-induced cerebral ischemia injury. This investigation might reveal the molecular mechanism of hyperglycemia-induced cerebral ischemia injury and thereby help to provide theoretical basis for seeking an effective treatment for perioperative cerebral ischemia.