杨腊邓月琴黄荣华郑涛刘丰李建明△.TRP 对KA 诱导的AD 模型大鼠学习记忆的影响及其作用机制[J].,2012,12(25):4816-4819 |
TRP 对KA 诱导的AD 模型大鼠学习记忆的影响及其作用机制 |
Effects of Triptolide on Learning and Memory and its Mechanism onAD Rats Induced by KA |
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DOI: |
中文关键词: KA Triptolide 学习和记忆 Morris 水迷宫 海马 |
英文关键词: Kainic acid Triptolide Learning and memory Morris Water Maze Hippocampus |
基金项目:湖南省自然科学基金项目(11JJ5072);湖南省科技计划项目(2010FJ4118/2011SK );湖南省医药卫生科研计划课题(B2011-071);
湖南省教育厅科学研究项目(11C0146);湖南省大学生创新实验项目(374) |
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中文摘要: |
目的:观察雷公藤甲素(Triptolide,TRP)对海人藻酸(Kainic acid,KA )海马内注射后大鼠学习记忆的影响及其作用机制。方法:
采用Morris 水迷宫筛选空间学习记忆能力正常的SD 雄性大鼠90 只(200~220g)。将实验动物分成3 组:右侧海马注射生理盐水
后生理盐水灌胃对照组(NS+NS)、右侧海马注射海人藻酸后生理盐水灌胃干预组(KA+NS)、右侧海马注射海人藻酸后雷公藤甲
素灌胃干预组(KA+TRP)。动物存活1 天,3 天,5 天,7 天,14 天,每个时间点6 只,处死前分别于各相应时间点用Morris 水迷宫
检测各组动物空间位置记忆能力;免疫组织化学方法结合图像分析技术检测海马CA1 区神经元COX-2 的表达。结果:与NS 组
(NS+NS)比较,KA 组(KA+NS)大鼠逃避潜伏期延长(P<0.05),跨越原平台次数减少(P<0.05);海马CA1 区的神经元COX-2 表达升
高(P<0.05);TRP 组(TRP+KA)与KA 组比较,大鼠的平均逃避潜伏期从第5 天起缩短(P<0.05),跨越原平台次数增多(P<0.05),
海马CA1 区神经元COX-2 表达在5 天,7 天时下调(P<0.05)。结论:KA 海马内注射,可以导致大鼠学习记忆功能障碍及上调海
马CA1 区神经元COX-2 表达;雷公藤甲素干预治疗,能够改善动物的学习和记忆能力,能抑制KA 诱导的海马CAl 区神经元
COX-2 的表达。 |
英文摘要: |
Objective: To observe the effects of triptolide (TRP) on learning and memory of rats induced by injection of kainic into
hippocampus and its mechanism. Methods: 90 SD rats with normal learning and memory were selected by Morris water maze method,
and then divided randomly into three groups: NS treated after NS injection into the right dorsal hippocampus group (NS+NS, n=30); NS
treated after KA injection into the right dorsal hippocampus group (KA+NS, n=30); TRP treated after KA injection into the right dorsal
hippocampus group (KA+TRP, n=30). The animals were sacrificed at d1, d3, d5, d7, d14 after KA injection, 6 rats for each time point.
The behavior of rats was detected by Morris water maze before sacrificed. COX-2 expression in CA1 region of hippocampus was investigated
by immunohistochemistry and computer image analysis methods. Results: Compared with that of NS+NS group, a significant increase
in the mean escape latencies of rats and an obvious decrease in frequency of passing through the platform of rats occurred in
KA+NS group (P<0.01). COX-2 expression of CA1 hippocampus obviously increased in KA+NS group (P<0.01). Compared with
KA+NS group, the mean escape latencies of rats decreased and the frequency of passing through the platform of rats increased at d 5, d 7,
d 14 in KA+TRP group (P<0.05). COX-2 expression in CA1 hippocampus significantly decreased at d 5, d 7 in KA+TRP group (P<0.
05). Conclusion: Kainic acid can contribute to the decreased learning and memory and the increased expression of COX-2 in area CA1 of
the hippocampus in vivo. Treatment with tritolide can inhibit the expression of COX-2 which was induced by kainic acid in CA1 area of
hip- pocampus. |
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