脑缺血是当今世界致残、致死率最高的疾病之一，目前仍缺乏有效的治疗手段。因此，寻找新的抗脑缺血靶点至关重要。神经元型一氧化氮合酶羧基末端PDZ配体（CAPON）的C-末端多肽可通过抑制PSD-95与神经元型一氧化氮合酶（nNOS）的结合来阻断NMDA受体/ PSD-95/ nNOS信号通路，而该信号通路诱导的nNOS过度激活是脑缺血诱发神经元死亡的重要原因。由此我们推测,CAPON可能对脑缺血具有重要的调控作用。迄今，还没有关于CAPON对脑缺血作用的相关报道。本课题着眼于CAPON，通过multicolor BiFC、病毒感染等方法，研究CAPON在脑缺血中的作用及其分子机制，并判断CAPON能否成为一个新的抗脑缺血靶点。

Although cerebral ischemia is one of the diseases which have the highest mutilation and fatality rate in the world, there has not an effective therapeutic method. So, it's important to look for new target. The polypeptide coming from the C-extremity of CAPON can block the NMDA receptor/ PSD-95/ nNOS signal pathway by inhibiting the binding of nNOS to PSD-95. The overactivation of nNOS by this signal pathway is an important reason for neuron death after cerebral ischemia. According to these results, we conclude that CAPON may play an important role in cerebral ischemia. Up to now, there isn't any report about the effect of CAPON on cerebral ischemia. With CAPON as the starting point, by means of multicolor BiFC, virus infection and so on, we will study the effect of CAPON on cerebral ischemia and its mechanism and determine if CAPON is a new target in the treatment of cerebral ischemia.