MicRNA-124可能通过PI3K/Akt通路调节缺血脑组织细胞凋亡  

MicRNA-124 may regulating hypoxia brain cells apoptosis through PI3K/Akt pathway

作　　者：王长明[1] 蒋国红[1] 徐平[1] 张金菊[1] 刘海军[1] 魏志杰[1] 张丽[1] 

机构地区：[1]遵义医学院附属医院神经内科,贵州遵义563003

出　　处：《中风与神经疾病杂志》2016年第2期146-149,共4页Journal of Apoplexy and Nervous Diseases

基　　金：遵义市科技计划;遵市科合社字(2014;No.78)

摘　　要：目的探讨脑缺血环境下对micRNA-124表达的影响。方法采用Western blot、荧光定量PCR技术检测脑缺血后缺血皮质区不同时间点bax、bcl-2、caspase-3、ROCK1、micRNA-124蛋白或基因的表达水平。结果缺血脑组织细胞micRNA-124基因表达量与调控细胞凋亡指标bax、bcl-2、caspase-3增高一致;bax、bcl-2、caspase-3、ROCK1活化片段蛋白表达量逐渐升高,在随后观察的时点内持续处于高表达状态(P<0.01)。结论 micRNA-124可能参与缺氧致脑组织细胞凋亡的过程,其机制可能是通过PI3K/Akt通路,激活或抑制bax、bcl-2、caspase-3、ROCK1其中一个或是多个基因调节缺氧脑组织细胞凋亡。Objective To explore micRNA-124 expression under the condition of cerebral ischemia. Methods Using Western blot and fluorescence quantitative PCR technique to detect bax,bcl-2,caspase 3,ROCK1,micRNA-124 protein or gene expression of ischemic cortex at different time points after cerebral ischemia. Results Gene expression of MicRNA-124 with bax,bcl-2,caspase-3 increased consistently; bax,bcl-2,caspase-3 and ROCK1 segments of activated protein expression quantity increased. In the subsequent observation point inside the continued at a high expression. Conclusion MicRNA-124 may be involved in the process of anoxia brain tissue cell apoptosis,its mechanism may be through PI3 K / Akt pathway to activate or inhibit bax,bcl-2,caspase-3,ROCK1 one or multiple genes,regulating cell apoptosis of the anoxia brain tissue.

关 键 词：micRNA-124 ROCK1 WESTERN BLOT 荧光定量PCR 细胞凋亡 

分 类 号：R743.32[医药卫生—神经病学与精神病学]