S-oxiracetam ameliorates ischemic stroke induced neuronal apoptosis through up-regulating α7 nAChR and PI3K / Akt / GSK3β signal pathway in rats. (May 2018)

• Record Type: Journal Article
• Authors: Fan, Wenxiang; Li, Xiang; Huang, Liangliang; He, Shucheng; Xie, Zhicheng; Fu, Yuxin; Fang, Weirong; Li, Yunman
• Is Part Of: Neurochemistry international. Volume 115(2017)
• Page Start: 50
• Page End: 60
• Publication Date: 2018-05
• Subjects: Ischemic stroke -- Apoptosis -- S-oxiracetam -- α7 nAChR -- GSK3β; Neurochemistry -- Periodicals; Neurochemistry -- Periodicals; Neurochimie -- Périodiques; Neurochemistry; Periodicals; 612.804205
• DOI: 10.1016/j.neuint.2018.01.008
• Languages: English
• ISSNs: 0197-0186

Abstract

Abstract: 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. Highlights: The effects of S-ORC on ischemic stroke. The possible mechanism is related to inhibiting apoptosis. The molecular mechanism is via α7 nAChR signal.