自发性蛛网膜下腔出血（SAH）患者常伴有认知障碍，其原因是SAH急性期全脑缺血缺氧状态引发的海马神经元凋亡及坏死。研究表明，SAH后神经元会启动自噬性保护机制以抵御神经元损伤。我们前期研究发现，在SAH模型大鼠急性期应用JSI-124可促进海马神经元自噬，预防认知障碍发生。但自噬是一把双刃剑，过度应用促自噬药物会造成大量神经元的自噬性死亡，加重SAH后的认知障碍。为此，本研究拟依据SAH大鼠脑脊液中LC3B反映的自噬水平，深入探讨SAH后海马神经元自噬的变化规律，应用认知功能检测实验确定SAH模型大鼠认知障碍的程度，找出JSI-124干预自噬的最佳时机和用药剂量与疗程，以验证我们提出的“适时与适度”上调自噬改善SAH后认知功能的假说；并阐明JAK2/STAT3和AMPK/mTOR通路在JSI-124促进海马神经元自噬中的作用。该研究有助于改善SAH患者认知功能，具有重要的学术和临床价值。

Patients suffering from subarachnoid hemorrhage (SAH) are poor prognosis, and cognitive deficiency generally ensues. This cognitive disorder due to the apoptosis and necrosis of hippocampal neuron, which result from the hypoxic-ischemia microenvironment. Recent studies have discovered that autophagy might play a pro-survival role in the mechanism of neuron damage after SAH. In our previous research, the application of JSI-124, a drug of natural extraction, significantly induced neuronal autophagy in the rat model of SAH, in which way the cognitive deficiency was avoided. However, as a “double-edged sword”, autophagy could lead to excessive cell death caused by overdose of pro-autophagy drugs, thus exacerbating the cognitive functions following SAH. Our research intend to explore the autophagy-related phenomena based on monitoring LC3B expression in cerebrospinal fluid after SAH of rat model and discuss the fluctuations of cognitive functions via tests of neuroethology. The proper occasion, dosage and course of JSI-124 intervening in SAH are then to be established through the experiments as well as the determination of the role of JAK2/STAT3 and AMPK/mTOR pathways in the hippocampal neuronal autophagy. Results would favor the hypothesis we presented that “appropriate and moderate regulation of autophagy” could positively improve cognitive function after SAH, which would reveal high academic value and provide new clinical strategy for SAH treatment.