血脑屏障在维持神经血管单元微环境的平衡和稳态中发挥重要作用，但脑缺血后血脑屏障结构功能损伤的具体分子机制目前仍不清楚。炎症反应与血脑屏障的破坏及功能障碍密切相关，互为因果，在脑缺血的病理过程中具有重要作用。既往研究表明，双孔钾通道TREK-1(TWIK- related potassium channel-1)参与内皮细胞粘附因子的表达，白细胞浸润等，在炎症诱导的血脑屏障破坏及功能失调中发挥重要作用。我们前期采用转基因小鼠模型研究发现TREK-1参与脑缺血后血脑屏障通透性的改变，炎症细胞浸润及炎性因子表达，因此本项目拟进一步从分子、细胞、整体水平研究TREK-1在脑缺血后血脑屏障结构破坏及功能失调中的具体作用，并进一步探讨其涉及的信号分子机制，为脑缺血神经保护的研究提供新的理论依据及干预靶点，为开发新的神经保护药物奠定理论基础。

The blood-brain barrier (BBB) plays an instrumental role in microenvironment homeostasis of neurovascular unit. However, the underlying mechanisms of BBB injury remain unclear. Brain inflammation can both cause and result from BBB dysfunction. Previous research have showed that TREK-1(TWIK- related potassium channel-1) is key in inflammation-related BBB dysfunction through downregulation of the expression of cellular adhesion molecules, and leukocyte trafficking into CNS. In our preliminary study, we found that TREK-1 influenced BBB permeability, leukocytes infiltration and expression of inflammatory cytokines after focal ischemia. In the present research, we would investigate the role of TREK-1 on BBB dysfunction after cerebral ischemia and the underlying mechanism in vitro and in vivo using TREK-1 knockout mice. Our research result will offer a new therapeutic intervention and theoretical basis for the treatment of ischemic stroke.