脑缺血/再灌注损伤细胞凋亡中JNK信号通路及抑制剂SP600125的作用  

Effects of JNK Signaling Pathway and SP600125-JNK Inhibitor in Apoptosis on Brain Ischemia Reperfusion

作　　者：许秀洪 吴春晓[1] 王娇[1] 周国平[1] 

机构地区：[1]南方医科大学中医药学院,广州510515

出　　处：《医学综述》2015年第9期1554-1556,共3页Medical Recapitulate

基　　金：国家自然科学基金(81173355)

摘　　要：c-jun氨基末端激酶(JNK)信号转导通路是细胞内作用蛋白网络的重要一环,参与胞外信号从细胞表面转导到细胞内部的过程,可被多种因素激活,在细胞的增殖与分化、形态维持、骨架构建和细胞凋亡等生物反应过程中发挥重要作用。脑缺血/再灌注损伤导致的细胞凋亡与丝裂原活化蛋白激酶家族有密切的关系,其中JNK信号通路是脑缺血/再灌注损伤中神经元凋亡进程的主要机制之一。大量实验提示,JNK信号转导通路及其抑制剂SP600125在脑缺血/再灌注损伤诱导的细胞凋亡中起重要的调控作用,应用JNK阻断剂可起到神经保护作用,通过对这些信号转导通路的组成及调节机制的研究,有望为临床上脑缺血疾病的治疗提供新的分子治疗靶点。c-Jun N-terminal kinase （JNK） signal pathway is one of the most important aspects of protein network in the cell and participates in the extracellular signal transduction from the cell surface to the internal process,could be activated by a variety of factors and played a role in cell proliferation and differentiation,cell maintaining, skeleton building and apoptosis. Cerebral iscbemia-reperfusion injury would cause apoptasis,which are closely related with the MAP/（ family. Besides, JNK signaling pathway is one of the main mechanisms of neuronal apoptosis process which caused by cerebral isehemia-reperfusion injury. Many studies show that JNK signal pathway and SP600125-JNK inhibitor plays an important regulation role in in apoptosis on brain isehemia reperfusion. Experimental results demonstrate that the application of JNK inhibitor may play a neuroprotective effeet. To study the composition and regulation mechanisms of these signaling pathways, which are expected to provide new molecular therapeutic tarlzets for the clinical treatment of cerebral ischemic diseases.

关 键 词：脑缺血/再灌注损伤 丝裂原活化蛋白激酶信号通路 c-Jun氨基端激酶信号通路 细胞凋亡 

分 类 号：B332[哲学宗教—外国哲学] R322.61[医药卫生—人体解剖和组织胚胎学]