对INT-FAK信号通路调控脑缺血后神经细胞凋亡的思考  

The Thinking of INT-FAK Signaling Pathway in Regulation of Neural Cell Apoptosis After Cerebral Ischemia

作　　者：陈昱文[1,2] 刘旺华[1,2,3] 陈娉婷[1,2] 曹泽标 金梦[1,2] 颜艳艳[1,2] 周小青[1,2,3] 

机构地区：[1]湖南中医药大学,湖南长沙410208 [2]湖南中医药大学中医诊断学湖南省重点实验室,湖南长沙410208 [3]湖南中医药大学数字中医药协同创新中心,湖南长沙410208

出　　处：《湖南中医药大学学报》2017年第1期106-110,共5页Journal of Hunan University of Chinese Medicine

基　　金：国家自然科学基金(81473567、81373702、81202632);教育部博士点基金(20124323120003);湖南省自然科学基金(13JJ3097);湖南省教育厅科研项目(14B134)

摘　　要：脑缺血性疾病是人类健康的主要杀手之一,相关研究表明,神经细胞的凋亡是造成脑缺血疾病中神经系统损害的主要机制之一,而以整合素-黏着斑激酶(INT-FAK)控制调节的PI3K/PDK/Akt以及Raf/MEK/ERK两条主要信号途径引起的细胞凋亡是其主要作用机制。凋亡过程出现的诸多能加以调控的信号分子,都可以作为治疗脑缺血性损伤的潜在靶点。随着对脑缺血损伤与神经细胞凋亡关联的深入研究,抗凋亡治疗已经成为治疗脑缺血性疾病的重要途径。Cerebral ischemia has been one of the killers in human health. The studies found that the apoptosis of neurons is an important mechanism leading to cerebral ischemia injury. Its main mechanism is the cell apoptosis caused by two siganal pathways：PI3K/PDK/Akt and Raf/MEK/ERK which were regulated by INT-FAK. The large number of adjustable signal molecules which exist in apoptosis, it can be used as a potential target for the treatment of cerebral ischemic injury.With the intensive study on the relationship between neurons apoptosis and cerebral ischemia, anti-apoptotic therapies have been the valuable methods.

关 键 词：脑缺血 细胞凋亡 PI3K/PDK/Akt信号通路 Raf/MEK/ERK信号通路 

分 类 号：R743[医药卫生—神经病学与精神病学]