摘要
脑缺血时，N-甲基-D-天门冬氨酸受体（NMDA—R），尤其是NR2B通过酪氨酸或丝／苏氨酸磷酸化作用其结构和功能发生改变，激活下游细胞信号传导通路，诱导神经元兴奋毒性、细胞凋亡。其受体和非受体酪氨酸激酶途径受金属离子、细胞因子、氧化应激、原癌基因等的调节。NMDA—R拮抗剂单独用药时可产生封顶效应，而联合用药可产生更强的神经元保护作用。
During cerebral ischemia, N-methyl-D-aspartate receptor （NMDA-R）, especially NR2B subunit, changes its structure and function via tyrosine or serine/threonine phosphorylation, and activates the downstream signal pathways to induce excitatory neurotoxicity and cell apoptosis. These pathways including receptor and non-receptor tyrosine kinase pathways are mediated by metallic cations, cytokines, oxidative stress, oncogene/pro-oncogene etc. NMDA-R antagonist exhibits ceiling effect when administered alone, and exerts much stronger neuron protection if combined with other therapia.
出处
《国际麻醉学与复苏杂志》
CAS
2007年第1期88-91,共4页
International Journal of Anesthesiology and Resuscitation
关键词
NMDA受体
脑缺血
NMDA receptor
cerebral ischemia
