摘要
目的 :探讨单唾液酸四己糖神经节苷酯 (GM1)在脑缺血再灌注损伤中的神经保护作用及其机制。方法 :仿照Pulsinelli四血管闭塞法 (4VO)建立大鼠全脑缺血再灌注损伤模型。实验分成三组 :假手术组、急性缺血再灌注组、GM1治疗组。应用微透析技术动态收集脑细胞外液。实验结束取出脑组织 ,制成切片。色谱法检测透析液的谷氨酸、天门冬氨酸。结果 :急性缺血再灌注组、GM1治疗组谷氨酸、天门冬氨酸基础水平与假手术组基本相同 ,缺血后即迅速升高 ,再灌注 30min达高峰 ,其后逐渐下降。再灌注组在 30~ 12 0min内显著高于对照组 (P <0 .0 5 ) ,治疗组在 30~ 90min内显著高于对照组 ,但低于再灌注组 (P <0 .0 5 )。结论 :①缺血再灌注损伤引起的神经损害与兴奋性氨基酸有关 ;②早期使用GM1治疗对脑缺血再灌注损伤有明确的保护作用 ,其机制与抗兴奋性氨基酸毒性有关。
Objective: To investigate the neuroprojective effects of GM1 on rat global cerebral ischemic reperfusion damage. Method: Pulsinelli’s method was employed to establish cerebral ischemia reperfusion animal model. The dynamic varieties of Glu and Asp were observed after giving exogenous GM1. Result: Basic levels of Glu and Asp in acute ischemia and reperfusion group and GM1 group were same as sham group’s. They improved swiftly after lack blood, and reached peak after the brain reperfusion 30 min, then gradually fell. The levels of acute ischemia and reperfusion group were sigmificantly higher than sham group’s in 30~120 min(P<0.05). The levels of GM1 group were notability higher than sham group’s, and lower than acute ischemia and reperfusion group’s in 30~90 min(P<0.05).Conclusions:① Neurodamage frome cerebral ischemia and reperfusion has nexus with Excitatory Amino Acids;② After cerebral ischemia and reperfusion, GM1 is use to neurodamage from Excitatory Amino Acids.
出处
《河北医学》
CAS
2004年第10期909-913,共5页
Hebei Medicine