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| 调心方有效部位和EGb761对Aβ双侧杏仁核注射致痴呆大鼠APPmRNA、Aβ阳性神经元和乙酰胆碱脂酶作用比较 |
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杨戈1, 李美华2, 金红姝3, 郁志华3, 张钦传3, 林水淼3
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1.北京中国中医研究院西苑医院, 北京, 100091;2.云南省昆明钢铁总公司职工医院八街分院, 昆明, 650303;3.上海市中医老年医学研究所, 上海, 200032
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| 摘要: |
| [目的]研究调心方有效部位(TX0201)和达纳康(EGb761)对β-淀粉样蛋白25-35(Aβ25-35)所致类老年性痴呆(AD)模型大鼠胆碱能系统作用的异同。[方法]采用双侧杏仁核注射Aβ25-35造成类AD大鼠模型,观察大鼠Morris水迷宫空间记忆能力、乙酰胆碱(AchE)活性,并分别通过逆转录多聚酶链反应(RT-PCR)和免疫组化方法研究类AD大鼠淀粉样前体蛋白(APP)mRNA表达和Aβ阳性神经元。[结果]1)类AD模型大鼠Morris水迷宫测试出现空间记忆能力下降,海马AchE含量降低,皮层、海马APPmRNA的表达上调,Aβ阳性神经元增加;2)TX020和EGb7611可以改善类AD大鼠空间记忆能力;下调海马APPmRNA的表达。[结论]TX0201和EGb761显著改善Aβ诱导的痴呆模型大鼠学习记忆障碍,可能是通过降低海马APPmRNA表达发挥作用。 |
| 关键词: 老年性痴呆 调心方有效部位 β淀粉样蛋白 乙酰胆碱 |
| DOI：10.11656/j.issn.1672-1519.2006.01.04 |
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| 基金项目:国家自然科学基金重点项目(39830450) |
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| Effect of TX0201 and Egb761 on APPmRNA,Aβ-positive Neuron and AChE in Rat with Alzheimer’s Disease Induced by Bilateral Injection of Aβ Corpus Amygdaloideum |
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YANG Ge1, LI Mei-hua2, JIN Hong-shu3
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1.The Xiyuan Hospital of China Academy of TCM, Beijing 100091, China;2.The Worker’s Hospital, Kunming General Company of Iron and Steel, Kunming 650303, China;3.Shanghai Institute of Gerontology with TCM, Shanghai 200032, China
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| Abstract: |
| [Objective] To research the mechanism of TX0201 Active position of Tiaoxin prescription(heart-regulating prescription)and EGb761(Danakang)on cholinergic system in rat with Alzheimer’s disease(AD).[Methods] AD was induced by Ab25-35 injected into the bilateral corpus amygdaloideum to observe the spatial learning and memory ability,AChE activity,and the expression of β-amyloid and β-amyloid precursor protein(APP)by RT-PCR and immunohistochemistry in the brain of the animal.[Results] In rats with AD the spatial learning and memory ability was damaged significantly,AChE activity decreased in its hippocampus.The expression of β-amyloid and APP mRNA increased in the cortex and hippocampus.TX0201 could improve the spatial learning and memory disturbance,decreased the expression of APP mRNA in hippocampus.[Conclusions] The TX0201 and EGb761 may obviously improve the learning and memory handicap of rats with AD by decreasing the expression of APP mRNA in hippocampus. |
| Key words: Alzheimer’s disease TX0201 β-amyloid protein acetylcholine |
