突触后密度
缺血
突触后电位
NMDA受体
兴奋毒性
冲程(发动机)
神经保护
脑损伤
受体
医学
一氧化氮
神经科学
心脏病学
内科学
生物
工程类
机械工程
作者
Shi-Fu Mo,Gao-Yong Liao,Jie Yang,Mengyu Wang,Yang Hu,Guoning Lian,Ling-Dong Kong,Yong Zhao
出处
期刊:Brain Research
[Elsevier BV]
日期:2016-10-01
卷期号:1648: 250-256
被引量:19
标识
DOI:10.1016/j.brainres.2016.07.012
摘要
Stroke is a major public health problem leading to high rates of death and disability in adults. Coupling of postsynaptic density protein-95 (PSD-95) and neuronal nitric oxide synthase (nNOS) plays an important part in neuronal damage caused by stroke. Recent studies suggest the possibility of alleviating post ischemia neuron damage by blocking ischemia-induced nNOS-PSD-95 association. Here, we report a small-molecular inhibitor of nNOS-PSD-95 interaction, SCR-4026, which exhibits neuroprotective activities in NMDA-induced or Oxygen and glucose deprivation (OGD)-induced neuronal damage in primary cortical neurons cultures, and ameliorated focal cerebral ischemic damage in rats subjected to middle cerebral artery occlusion (MCAO) and reperfusion. Furthermore, we found that SCR-4026 was also able to promote neural stem cells to differentiate into neurons-like cells, which is potentially of great significance for neural protection. Taken together, SCR-4026 is identified as a novel small molecule that shows great potential in treating stroke.
科研通智能强力驱动
Strongly Powered by AbleSci AI