脑卒中是严重威胁人类生命和健康的疾病，早期溶栓是临床唯一有效的治疗方案，但治疗窗窄，且对后期神经修复、功能重建无直接作用。我们在前期工作中已经证明了阻断nNOS-PSD95对脑缺血的急性损伤保护作用，本项目拟以nNOS-PSD95、nNOS-CAPON相互作用为切入点，研究这两个靶点在延迟治疗中对运动功能和学习记忆能力，对星型胶质细胞激活和疤痕形成，对树突重构和突触可塑性的影响，以及相关的分子机制，从而阐明nNOS与转接蛋白相互作用在脑卒中神经功能重建中的意义。本项研究将有助于延长脑卒中治疗时间窗，发现促进神经功能修复的治疗靶标。

Stroke is a major cause of death and acquired disability in adults. Thrombolysis in the first several hours is the only approved treatment in clinic, but the therapeutic window is very narrow and thrombolysis can not promote neural rehabilitation and functional rebuilding directly. We have demonstrated the neuroprotection by disrupting nNOS-PSD95 interaction after cerebral ischemia. In this project, we will investigate the effects of delayed disrupting nNOS-PSD95 or nNOS-CAPON interaction after ischemic stroke on the motor function and spatial learning and memory, reactive astrocytes and glial scars, and dendrite and synapse plasticity. Moreover, we will explore the underlying mechanisms too. So this project will reveal the role of protein interaction with nNOS in functional rebuilding after stroke, helping extend the therapeutic window and discover novel targets for neural repair.