摘要
[目的]观察脑缺血再灌注后大鼠皮质谷氨酸(Glu)含量及N-甲基-D-天冬氨酸(NMDA)受体活性变化,旨在探讨通脉注射液对缺血性中风后兴奋性毒性作用可能的干预机制。[方法]采用四血管结扎全脑缺血再灌注模型,以放免法测定皮质中Glu和NMDA受体的活性,观察脑缺血后Glu和NMDA受体变化及比较通脉注射液对二者的影响。[结果]脑缺血再灌注模型组皮质Glu含量显著升高、NMDA受体活性上升,通脉注射液组大鼠皮质Glu的含量和NMDA受体活性与模型组比较显著降低。[结论]脑缺血再灌注后兴奋性毒性作用产生,以黄芪和益母草为主的通脉注射液能够通过减弱缺血再灌注后的兴奋性毒性过程,从而起到保护脑皮质的作用。
[Objective] To explore the counteractive mechanism of Tongmai Injection (IT) for excitotoxicity in rats with cerebral ischemia/reperfusion by observing the glutamic acid (Glu) content and N-methyl-D-aspartate (NMDA) receptor activity in rats cortex. [ Methods ] Rat models with cerebral ischemia/reperfusion were established by four-vessel occlusion. Glu content and NMDA receptor activity were examined by radioimmunoassay and the effects of TI on Glu and NMDA receptor were also observed. [ Results ] Glu content and NMDA receptor activity were both increased in the model group and TI could counteract the above changes. [Conclusion] Cerebral ischemia/reperfusion can induce excitotoxicity and TI can protect the cerebral cortex.
出处
《广州中医药大学学报》
CAS
2003年第3期227-229,239,共4页
Journal of Guangzhou University of Traditional Chinese Medicine
关键词
通脉注射液
脑缺血
再灌注
大鼠
兴奋性毒性作用
干预机制
放射免疫法
TONGMAI INJECTION/pharmacology
CEREBRAL ISCHEMIA/TCD therapy
ASTRAGALUS MEMBRANACEUS/ther. use
LEONURUS HETEROPHYLLUS/ther. use
GLUTAMIC ACID/analysis
RECEPTORS, N-METHYL-D-ASPARTATE
