中国康复理论与实践2016，Vol.22Issue(6)：621-628,8.DOI:10.3969/j.issn.1006-9771.2016.06.001
卒中后认知障碍小鼠胆碱能神经环路组蛋白乙酰化内稳态失衡的机制研究
Change of Histone Acetylation Homeostasis of Central Cholinergic Circuits in Mice with Post-stroke Cognitive Impairment
摘要
Abstract
Objective To observe the change of histone acetylation homeostasis of the central cholinergic circuits in mice with post-stroke cognitive impairment (PSCI). Methods The male ICR mice were divided into sham group (n=60) and PSCI group (n=60). The middle cerebral artery occlusion (MCAO) model was established. The Morris water maze test was used to test the cognitive function, and the changes of function and the histone acetylation homeostasis of the central cholinergic circuits of unaffected side were detected by molec-ular biology methods. Results Compared with the sham group, the scores of Morris water maze test decreased in PSCI group (t>29.412, P<0.05); while the acetylcholine (Ach) level decreased (t>26.227, P<0.05), as well as the expression of choline acetyltransferase (ChAT) mRNA and protein (t>28.593, P<0.05), acetylated histone H3 (Ac-H3) (t>24.126, P<0.05), phosphorylated cAMP response element-binding protein (p-CREB) and CREB binding protein (CBP) (t>25.634, P<0.05), and the acetylated histone level of M promoter of ChAT (t>24.704, P<0.05). Conclusion Transient MCAO could cause PSCI. The function of the central cholinergic circuits was impaired, especially the his-tone acetylation homeostasis of the central cholinergic circuits, such as the acetylated histone level of ChAT promoter decreased. All of that might be related with the decline of p-CREB and CBP level in the corresponding brain regions induced by stroke.关键词
卒中后认知障碍/胆碱能环路/乙酰胆碱/组蛋白乙酰化/cAMP反应元件结合蛋白/小鼠Key words
post-stroke cognitive impairment/cholinergic circuits/acetylcholine/histone acetylation/cAMP response element-binding protein/mice分类
医药卫生引用本文复制引用
王鑫,孙彩花,徐旸,朱小云,陈霞,施伟,杨敏..卒中后认知障碍小鼠胆碱能神经环路组蛋白乙酰化内稳态失衡的机制研究[J].中国康复理论与实践,2016,22(6):621-628,8.基金项目
国家自然科学基金项目(No.81301673)。 （No.81301673）
