血管性痴呆大鼠海马CA1区β淀粉样蛋白和Tau蛋白的表达及意义

发布时间：2018-06-21 11:47

本文选题：血管性痴呆 + 水迷宫　；参考：《广西医科大学》2012年硕士论文

【摘要】：目的①本研究通过结扎大鼠双侧颈总动脉,建立血管性痴呆动物模型；②观察脑缺血后不同时间大鼠行为学、病理学变化；③研究大鼠脑缺血后不同时间点β淀粉样蛋白和Tau蛋白表达以及缺血性脑血管病与血管性痴呆(VD)的关系。并探讨β淀粉样蛋白和Tau蛋白在VD大鼠发生、发展中的表达及意义。方法采用永久性结扎大鼠双侧颈总动脉方法建立VD模型。40只SD大鼠采用随机分为假手术组(10只)、VD模型组(30只)。模型组大鼠按手术时间又分为4W、6W、8W组(每组n=10)。应用Morris水迷宫检测大鼠的学习、记忆能力；免疫组化染色方法检测大鼠海马CA1区β淀粉样蛋白和Tau蛋白的表达；用HE染色观察各组大鼠海马CA1区神经元数目的变化。结果与假手术组比较,模型组大鼠术后4、6、8周学习记忆能力明显下降,差异有统计学意义(P0.05)。随缺血时间的延长,大鼠学习记忆能力减退越明显,4W时最明显。HE染色显示手术组海马CA1区细胞排列疏松,数目减少,细胞形态异常。免疫组化显示痴呆组大鼠海马CA1区p淀粉样蛋白和Tau蛋白的表达于缺血4周时表达增加最明显,6W和8W表达缓慢下降,但与假手术组比较表达仍处于较高水平,差异均具有统计学意义(P0.05)。说明脑缺血损伤后可以导致脑组织Aβ蛋白含量增加和Tau蛋白的过度磷酸化,提示脑缺血损伤具有导致VD病理基础。结论采用双侧颈总动脉结扎法可使大鼠学习记忆功能明显减退,可成功建立血管性痴呆大鼠模型。VD大鼠认知功能、记忆功能减退与Aβ和Tau蛋白表达增加有关,并可能参与缺血后海马神经元的损害,是构成血管性痴呆的机制之一
[Abstract]:Objective 1 the purpose of this study was to establish a vascular dementia animal model by ligating bilateral common carotid arteries to observe the behavioral and pathological changes in rats at different time points after cerebral ischemia. 3To study the expression of 尾 -amyloid protein and Tau protein at different time points after cerebral ischemia in rats and the relationship between ischemic cerebrovascular disease and vascular dementia (VD). To investigate the expression and significance of 尾 -amyloid protein and Tau protein in the pathogenesis and development of VD rats. Methods VD model was established by permanent ligation of bilateral common carotid artery in rats. Forty SD rats were randomly divided into sham operation group (n = 10) and VD model group (n = 30). The rats in the model group were divided into 4 WX 6 W and 8 W groups according to the operation time (n = 10, n = 10). Morris water maze was used to detect the ability of learning and memory, immunohistochemical staining was used to detect the expression of 尾 -amyloid protein and Tau protein in hippocampal CA1 area of rats, and HE staining was used to observe the number of neurons in hippocampal CA1 area of rats. Results compared with the sham-operated group, the learning and memory ability of the model group decreased significantly at 6 weeks after operation, and the difference was statistically significant (P 0.05). With the prolongation of ischemic time, the learning and memory ability of rats decreased significantly at 4 W. He staining showed that the cells of hippocampal CA1 area in the operation group were loose, the number was decreased, and the morphology of the cells was abnormal. Immunohistochemical staining showed that the expression of amyloid protein and Tau protein in hippocampal CA1 area of dementia group decreased slowly after 4 weeks of ischemia, but the expression level was still higher than that in sham operation group. The difference was statistically significant (P 0.05). These results suggest that the increase of A 尾 protein content and the excessive phosphorylation of Tau protein after cerebral ischemia injury may lead to the pathological basis of VD. Conclusion bilateral common carotid artery ligation can significantly decrease the learning and memory function of rats, and can successfully establish vascular dementia rat model .VD rats' cognitive function. The decrease of memory function is related to the increased expression of A 尾 and Tau protein. It may be involved in the damage of hippocampal neurons after ischemia, which is one of the mechanisms of vascular dementia.
【学位授予单位】：广西医科大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R749.13

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