蛛网膜下腔出血（SAH）是一类具有高致残率，高致死率的脑血管疾病。研究证实自噬反应在SAH后早期脑损伤（EBI）中发挥重要的脑保护作用，Pannexin-1通道蛋白参与细胞内ATP胞外释放，继而激活AMPK/mTOR/ULK1自噬信号通路，可能在SAH后EBI中起脑保护作用。综上我们提出假说：Pannexin-1通道蛋白的开放，激活自噬反应，保护神经元细胞，改善SAH后EBI。为了验证该假说，我们采用腺相关病毒转染技术基因敲除和过表达Pannexin-1通道蛋白，利用实时定量PCR、免疫荧光染色、western blot等实验技术在大鼠体内体外SAH模型中观察Pannexin-1通道蛋白介导的自噬反应在SAH后EBI中的脑保护作用，同时验证Pannexin-1通道蛋白激活自噬反应的信号通路机制，为治疗SAH提供新的靶点和理论基础。

Subarachnoid hemorrhage (SAH) is known as a cerebrovascular disease with a high rate of mortality and disability. Recent advances in SAH research suggest that autophagy plays a protective role in the period of early brain injury (EBI) after SAH. Pannexin-1 channels release ATP into the extracellular space, which may activate the AMPK/mTOR/ULK1 mediated autophagy. We raised a hypothesis that activation of pannexin-1 channels could initiate the autophagy and protect the neurons from EBI after SAH. Pannexin-1 channels gene knockdown and overexpression were achieved by adenovirus associated virus (AAV) administration. In addition, quantitative real-time polymerase chain reaction (PCR), immunofluorescence staining and western blot were performed to explore the potential interactive mechanism between pannexin-1 channels and autophagy related neuroprotective effects on EBI after SAH in vivo and vitro study. There by providing a novel therapeutic target and theoretical basis for SAH treatment.