摘要
目的 研究二苯乙烯苷对脑缺血再灌注啮齿动物脑组织N 甲基 D 天 (门 )冬氨酸 (NMDA)受体结合力的影响 ,同时观察二苯乙烯苷对神经细胞内钙离子浓度的影响 ,初步探讨二苯乙烯苷对缺血再灌注动物的脑保护作用的机制。方法 麻醉后夹闭沙土鼠和小鼠双侧颈总动脉 10min后 ,小心撤去动脉夹制作缺血再灌注动物模型 :(1)沙土鼠再灌注 7d后处死 ,取前脑进行NMDA受体结合力实验 ;(2 )小鼠再灌注 15min后迅速断头取脑 ,切成脑片 ,加入Fluo 3/AM负载后 ,在激光扫描共聚焦显微镜上进行光切 ,观察不同层面皮层和海马区细胞内游离钙的荧光强度。结果 模型组的NMDA受体结合力比假手术组明显升高 ,而二苯乙烯苷治疗组可以降低模型动物的NMDA受体结合力 ;脑片的光切结果显示 ,脑缺血再灌注模型组神经细胞内游离钙离子浓度比假手术组明显升高 ;与模型组相比 ,二苯乙烯苷治疗组的细胞内游离钙离子浓度降低。结论 二苯乙烯苷能够抑制啮齿动物脑缺血再灌注所导致的脑组织NMDA受体结合力及神经细胞内钙离子浓度的升高 ,减轻钙超载导致的脑组织损伤 。
AIM To investigate the effects of tetrahydroxystilbene on binding force of NMDA receptors and concentration of intracellular calcium ions of nerve cell in brain ischemia reperfusion rodent and to explore the mechanism of protection of tetrahydroxystilbene on brain. METHODS Gerbil and mice's bilateral carotid arteries were occluded for 10 min after anesthesia and then reperfused to make ischemia reperfusion model:(1) Gerbils were sacrificed 7 d after reperfusion and the binding force of NMDA receptors of gerbil forebrain were assayed; (2)Mice were sacrificed 15 min after reperfusion and their brains were sliced. Fluo 3/AM was added into the slice and fluorescent intensity of intracellular free calcium in cortex and hippocampus area of different layer were observed through optical section of laser scanning confocal microscopy (LSCM). RESULTS Binding force of NMDA receptors of model group was significantly higher than that of sham operation group, while tetrahydroxystilbene treatment can decreased it significantly. Optical section result showed that calcium concentration in model group was higer than that of sham operation group. Compared with model group, the calcium concentration in the group treated with tetrahydroxystilbene was lower remarkably. CONCLUSION Tetrahydroxystilbene may relieve the increase of binding force of NMDA receptor and the raise of intracellular calcium ion concentration of rodent nerve cell caused by brain ischemia reperfusion, thus alleviate brain injure induced by calcium overload, and have protective effects on brain.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2003年第10期1112-1115,共4页
Chinese Pharmacological Bulletin
基金
国家重点基础研究发展计划"973"项目(NoG200 0 57010)
北京市科委资助首都"2 48"重大创新工程项目(H010 210 130113)
北京市重点科技实验室项目(No951890 60 0)
北京中医药管理局资助北京市中医药重点学科项目 (2 0 0 1)
