764-3对Alzheimer’s病样大鼠的治疗作用  被引量:6

Therapeutic effect of 764-3 on rat with Alzheimer's like disease

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作  者:张世仪[1] 陈艳[1] 左萍萍[1] 袁勃[1] 刘丹[1] 井艳玲[1] 刘燕[1] 

机构地区:[1]中国医学科学院基础医学研究所中国协和医科大学基础医学院,北京100005

出  处:《基础医学与临床》2001年第1期69-72,共4页Basic and Clinical Medicine

基  金:卫生部科研基金资助项目!(98 1 0 11)

摘  要:向大鼠侧脑室内注射聚集态的β 淀粉样多肽 (Aβ 2 5 35 ) 15mmol后 ,动物在三种行为试验中都出现学习记忆障碍 ,同时海马和大脑皮层的胆碱乙酰转移酶 (ChAT)活性下降。这表明应用Aβ 2 5 35脑室内注射造成Alzheimer’s病动物模型的可行性。 76 4 3于手术后早期多次给药 (2mg/ 0 5mL 每天 1次i p )明显改善Aβ 2 5 35所致的学习记忆缺陷 ,并使海马的ChAT回升。本文又首次报告Aβ 2 5 35引起前脑多个脑区的一氧化氮合酶(NOS)表达上调 ,76 4 3拮抗此反应。结果提示 76 4 3的作用机制与其在脑内提高ChAT活性和抑制病理性的NOS表达有关。Intracerebroventricular (icv) administration of aggregated beta amyloid peptide 25-35(Aβ 25-35, 15nmol) in rats induced learning and memory impairment in three behavioral tasks. Meanwhile, activity of choline acetyltransferase (ChAT) in hippocampus and cerebral cortex reduced. This demonstrates that Aβ 25-35 (icv) injection to produce a rat model for Alzheimers disease is feasible. Post surgery repeated treatment of 764 3 (2mg/day i p ) significantly improved learning and memory deficits caused by Aβ 25-35 and increased ChAT activity in hippocampus. Moreover, present study reported, for the first time, that Aβ 25-35 (icv) induced up expression of nitric oxide synthase (NOS) in several areas of forebrain and 764 3 blocked this response. Results suggest that mechanism of 764 3 treatment involves rise of ChAT activity and depression of NOS pathological expression in the brain.

关 键 词:β-淀粉样多态 阿尔茨海默病 丹参有效成分 764-3 治疗 实验研究 

分 类 号:R749.16[医药卫生—神经病学与精神病学]

 

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