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作 者:王伟斌[1] 宋春风[2] 吕佩源[1] 尹昱[1] 粱翠萍[1]
机构地区:[1]河北省人民医院神经内科,河北石家庄050051 [2]河北医科大学电镜实验中心,河北石家庄050017
出 处:《中国神经免疫学和神经病学杂志》2005年第6期337-339,共3页Chinese Journal of Neuroimmunology and Neurology
基 金:河北省自然科学基金资助项目(301415)
摘 要:目的观测缺血性小鼠额叶皮层和海马组织环磷酸腺苷(cAMP)水平,探讨脑缺血发病的分子生物学机制。方法通过双侧颈总动脉线结、连续3次缺血-再灌注制作脑缺血动物模型,并设立假手术组;术后29、30 d分别测试学习和记忆成绩;应用放射免疫法检测小鼠额叶皮层和海马组织cAMP水平。结果与假手术组比较,模型组学习和记忆成绩均降低(P<0.05),且额叶皮层和海马组织cAMP水平也降低(P<0.05)。结论额叶皮层和海马组织cAMP水平降低可能参与了脑缺血的分子生物学发病机制。Objective To observe the cAMP level in frontal cortex and hippocampus of mice with cerebral ischcmia, and explore the molecular pathogcncsis of cerebral ischemia. Methods The mice were subjected for ischemia-repcrfusion three timcs on bilateral common carotid arteries by knots to establish models of cerebral ischcmia and the changes of learning and memory wcrc tested on 29 d/30 d after operation. Shamed-operation mice were introduced as control group. The cAMP level was evaluated by the radioimmunoassay (RIA). Results Compared with shamed-operation group, the learning and memory of model group was worse (P〈0.05) and the cAMP level in frontal cortex and hippocampus was lower (P〈0. 05). Conclusions The lower cAMP level in frontal cortex and hippocampus might participate in the molecular pathogcnesis of cerebral ischemia.
分 类 号:R749.1[医药卫生—神经病学与精神病学]
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