Ischemic stroke, the main reason for severe disabilities in the world, is associated with a high incidence of sensorimotor and cognitive dysfunction. In this study, we use the middle cerebral artery occlusion/reperfusion (MCAO/R) model in rats and oxygen glucose deprivation/reoxygenation (OGD/R) model in fetal rat primary cortical neurons to investigate whether and how S-oxiracetam (S-ORC) protect brain injury from ischemic stroke. The results revealed that S-ORC reduced brain infarct size and lessened neurological dysfunction after stroke. Further study demonstrated that S-ORC diminished TUNEL positive cells, increased cell viability, decreased LDH activity, and inhibited cell apoptotic rate. Furthermore, S-ORC inhibited neuronal apoptosis by activating the PI3K/Akt/GSK3β signaling pathway via α7 nAChR, which was evidenced by α7 nAChR siRNA. In conclusion, our findings strongly suggest that S-ORC could be used as an effective neuroprotective agent for ischemic stroke due to its effect in preventing neuronal apoptosis.

缺血性中风是世界上严重残疾的主要原因，与感觉运动和认知功能障碍的高发有关。在这项研究中，我们使用大鼠的大脑中动脉闭塞/再灌注（MCAO / R）模型和胎儿大鼠原代皮层神经元的氧葡萄糖剥夺/复氧（OGD / R）模型来研究是否以及如何使用S-奥拉西坦（S- ORC）保护大脑免受缺血性中风的伤害。结果显示，S-ORC减少了中风后的脑梗死面积并减轻了神经功能障碍。进一步的研究表明，S-ORC可减少TUNEL阳性细胞，增加细胞活力，降低LDH活性，并抑制细胞凋亡率。此外，S-ORC通过激活经由α7nAChR的PI3K / Akt /GSK3β信号通路抑制神经元凋亡，这由α7nAChR siRNA证明。