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机构地区:[1]东南大学附属中大医院神经内科,南京210009 [2]复旦大学附属华山医院神经内科,上海200040
出 处:《国际脑血管病杂志》2006年第11期812-815,共4页International Journal of Cerebrovascular Diseases
摘 要:目的:探讨慢性脑低灌注对脑组织β淀粉样蛋白(Aβ)和细胞凋亡相关指标表达的影响。方法:SD大鼠20只随机分为二血管闭塞(2VO)模型组和假手术组,2VO模型大鼠永久性阻断双侧颈总动脉,造成脑部持续性低灌注;用Y-迷宫检测大鼠学习记忆能力,术后21d处死,用免疫组化方法检测大脑皮质、海马Aβ_(1-40)、Bax和Bcl-2表达。结果:2VO术后14d和21d学习记忆能力减退;2VO模型组大脑皮质和海马Aβ_(1-40)表达(分别为37.3±4.2和26.0±3.9)较假手术组(22.3±6.0和18.3±3.5)增加(P<0.01);2VO模型组Bax和Bcl-2表达较假手术组增加(P<0.01);Aβ_(1-40)与Bax/Bcl-2比值呈正相关(P=0.70)。结论:2VO术后脑内Aβ表达增加,可能参与了脑缺血后痴呆的发生;Aβ调节Bax/Bcl-2比值,促进脑细胞凋亡,损害认知功能,引起痴呆。Objective: To explore the effect of chronic cerebral hypoperfusion on the expressions of β-amyloid (Aβ) and apoptosis related indicators in brain tissues. Methods: Twenty SD rats were randomly divided into two vascular occlusion (2VO) model group and sham-operated group. The permanent occlusion of bilateral carotid arteries of 2VO rat model caused persistent cerebral hypoperfusion. Learning and memory abilities in rats were assessed by the Y-maze test. The rats were killed 21 days after operation, and the expressions of cerebral cortex, hippocampal A13140, Bax, and Bcl-2 were detected by immunohistochemistry. Results: The learning and memory abilities of the rats declined at 14 and 21 days after 2VO. The expressions of cerebral cortex and hippocampal Aβ1-40 were higher in the 2VO model group (37.3 ± 4. 2 and 26.0 ± 3.9, respectively) than those in the sham-operated group (22.3 + 6.0 and 18.3 ± 3.5, P 〈 0. 01 ); the expressions of Bax and Bcl-2 in the 2VO model group were higher than those in the sham-operated group (P 〈 0.01 ). The ratios between Aβ1-40 and Bax/Bcl-2 showed a positive correlation (r = 0.70). Conclusiorn: The increased expression of Aβ in brain after 2VO may have participated in the occurrence of dementia after cerebral ischemia; Aβ may regulate the ratio of Bax/Bcl-2, contribute to apoptosis, damage cognitive function, and cause dementia.
关 键 词:脑低灌注 Β淀粉样蛋白 BAX BCL-2 大鼠
分 类 号:R749.16[医药卫生—神经病学与精神病学]
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