摘要
采用SD大鼠,通过应激的方法制备高血压模型,并在此基础上阻断一侧大脑中动脉(MCAO),造成局灶性脑缺血。观察了缺血后3、12、24h神经细胞膜Na+K+—ATPase活性的变化,同时观察了神经节苷脂GM1对其活性的影响。结果发现,随缺血时间的延长酶活性逐渐降低,GM1术前30min给药(10mg/kg)能明显抑制缺血后3h酶活性的下降,但对缺血后12、24h酶活性的下降无改善作用。提示GM1术前给药对缺血早期具有脑保护作用。
Changes in the activity of Na+K+ -ATPase and GM1 effects were studied on the stress induced hypertensive rat et 3,12,and 24hours following occlusion of middle cerebral artery(MCAO).The decreases in the enzyme activity was observed in the three grops.In the GM1 group,GM1(10mg/kg)was intraperitoneally injected 30 min. before occlusion,the decteases of Na+K+ -ATpase activity was signficantly attenuated in 3h group.It is suggested that the GM1 may protect function of cerebrum during the early phases of ischemic injury.
出处
《中风与神经疾病杂志》
CSCD
北大核心
1996年第2期66-68,共3页
Journal of Apoplexy and Nervous Diseases
基金
卫生部"八五"攻关资助
上海医大神经生物国家重点实验室资助