ATP敏感性钾通道（ATP sensitive potassium channel, K-ATP）是偶联细胞代谢和电活动的特殊钾离子通道，是机体重要的内源性保护机制之一。我们前期研究发现：K-ATP通道表达于脑内神经血管单元的各组分，且可调节脑卒中后神经血管单元的功能。因此，我们提出"K-ATP通道是调节神经血管单元功能的潜在靶标"的研究假说。本申请项目拟在整体、细胞和分子水平系统研究K-ATP通道开放剂对神经血管单元（重点关注胶质细胞和脑微血管）功能的调节作用及其对脑卒中进程的影响；阐明K-ATP通道开放剂在脑卒中后内源性神经保护中的重要作用；揭示K-ATP通道开放剂用于脑卒中治疗的时间窗效应。在项目的实施过程中，发现一些靶向于神经血管单元、对神经损伤多元病理机制和内源性保护机制具有调制作用的关键分子，为发展多潜能的神经保护剂提供新靶标和积累学术基础、为脑卒中的临床治疗提供有益的思路。

ATP sensitive potassium channels (K-ATP) are unique potassium channels that directly couple the metabolic state of a cell to its electrical activity. Our previous studies found that K-ATP channel expressed on the all components of neurovascular unit, and could regulate neurovascular unit functions. Based our primary results, we proposed that K-ATP channel should be a promise target for regulating neurovascluar unit. Firstly, the present project is planned to investigate the essential roles of K-ATP channel on the neurovascular unit and on the stroke processes. Secondly, we will demonstrate the impacts of K-ATP channel on the endogenous neuroprotective mechanisms after stroke. Thirdly, we will further reveal the therapeutical time window for stroke. The expected results would discover new promise targets for regulating neurovascular unit and for modulating multiple pathomechanisms and endogenous neuroprotection. And the expected fingdings would provide benefical therapeutical strategies for stroke.