p38丝裂素活化激酶与脑缺血性损伤关系的研究进展  

Research Progress of the Relationship between p38 Mitogen-activated Protein Kinase and Cerebral Ischemia

作　　者：顾莹辉[1] 刘宏顺[1] 戴海琳 冯姗姗[1] 冯雪丹[1] 

机构地区：[1]保定市第二医院神经内科,河北保定071000

出　　处：《医学综述》2011年第11期1624-1626,共3页Medical Recapitulate

摘　　要：丝裂素活化激酶(MAPK)级联信号转导途径是许多信号转导通路的整合点。许多酪氨酸激酶都可以通过刺激信号级联反应激活丝裂原活化蛋白激酶通路。p38 MAPK通路是MAPK家族主要成员之一。p38 MAPK在脑缺血后早期被激活,参与炎性反应、自由基损伤、细胞凋亡等病理、生理过程,在脑缺血神经元死亡过程中发挥重要的调控作用。p38 MAPK抑制剂可望成为脑缺血性损伤临床治疗的有效途径。Mitogen-activated protein kinase（MAPK） is an integration point of different signal transduction pathways.Many tyrosine kinases can be activated by stimulating the signaling cascade of MAPK pathway.p38 MAPK,as one of the major MAPK family member,is activated and plays an essential role in early stage of ischemic neuronal injury,involved in inflammatory response,cytokine secretion,cell apoptosis,playing an important regulating role in cerebral ischemia neuronal death.Inhibitor of p38 MAPK is expected to be a new effective clinical treatment for cerebral ischemia.

关 键 词：丝裂素活化激酶 p38丝裂素活化激酶 脑缺血性损伤 

分 类 号：R743.32[医药卫生—神经病学与精神病学]