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.
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
