皮质发育障碍模型鼠海马区神经元凋亡机制的研究  

Mechanism of apoptosis in hippocampus of the rats with disorder of cortical developments

作　　者：黄华[1] 冯占辉[1] 何选丽[1] 黄敏[1] 晏勇[1] 

机构地区：[1]重庆医科大学附属第一医院神经内科重庆市神经病学重点实验室,重庆400016

出　　处：《重庆医科大学学报》2009年第2期129-134,共6页Journal of Chongqing Medical University

基　　金：国家自然科学基金资助项目(30570636)。

摘　　要：目的:探讨皮质发育障碍(Disorder of cortical developments,DCDs)模型鼠海马神经元的凋亡机制。方法:利用卡莫司汀(BCNU)诱导建立SD大鼠皮质发育障碍动物模型,在出生后0d(P0)、15d(P15)、30d(P30)、45d(P45)和60d(P60)时,采用TUNEL检测海马区神经元凋亡,RT-PCR方法和免疫组化分别对8只模型鼠和正常鼠检测海马区Bcl-2和Bax的在mRNA和蛋白水平的表达,并结合图像分析系统进行结果分析。结果:成功建立SD大鼠皮质发育障碍动物模型;与对照组比较,TUNEL、免疫组化和RT-PCR检测结果显示:P0模型鼠组海马区神经元凋亡无明显变化,P15、P30、P45、P60模型组神经元凋亡逐渐加重,有显著差异(P<0.05),且随存活时间延长,模型组海马神经元Bax表达逐渐增强,Bax/Bcl-2比值较对照组增高,具有显著统计学意义(P<0.05)。结论:皮质发育障碍模型鼠海马区存在显著的神经元凋亡,Bcl-2和Bax参与了其凋亡过程;皮质发育障碍模型鼠海马神经元凋亡可能参与了皮质发育障碍所致的癫痫及难治性癫痫的发病机制。Objective：To study the mechanism of apoptosis in hippocampus of the rats with disorder of cortical developments. Methods： The Rats with disorder of cortical developments were established by carmustine （BUCN）. AT PO, P15, P30, P45, P60, the number of apoptosis cell and expression of Bax and Bcl-2 in hippocampus were detected by TUNEL, immunohistochemistry method and RT-PCR; then the detected outcomes were analyzed by computer micrograph analysis system in control group and model group. Results：At P15, P30, P45, P60, the numbers of apoptosis, Bax, Bcl-2 masculine cell and bcl-2 MRNA, bax MRNA in hippocampus in the model group were more than those in the control group. The ratio of Bax/Bcl-2 in model group was significantly higher than those in the control group （P〈0.05）, but at PO, they were not different. Conclusion： Apoptosis exist notably in hippocampus of rat with disorder of cortical developments, bcl-2 and bax probably play a role in apoptosis. Apoptosis may be associated with the pathogenesis of epilepsy or intractable epilepsy.

关 键 词：皮质发育障碍 细胞凋亡 BAX BCL-2 癫痫 

分 类 号：R742.1[医药卫生—神经病学与精神病学]