外伤性脑损伤后神经细胞保护因子表达的变化  

Changes of Nerve Cell Protective Factors After Traumatic Brain Injury

作　　者：范宇鸿 呼格吉乐[2] 高乃康[2] 兰海霞[3] FAN Yu-hong;HUGE Ji-le;GAO Nai-kang;LAN Hai-xia(Inner Mengolia Medical University,Hohhot 010059 China;The Affiliated Hospital of Inner Mongolia Medical University,clinical laboratory and neurosurgery,Hohhot 010050 China;The 253th Hospital of PLA,paediatrics,Hohhot 010000 China)

机构地区：[1]内蒙古医科大学 [2]内蒙古医科大学附属医院检验科神经外科,内蒙古呼和浩特010050 [3]中国人民解放军第253医院儿科,内蒙古呼和浩特010000

出　　处：《内蒙古医学杂志》2018年第7期793-795,共3页Inner Mongolia Medical Journal

基　　金：内蒙古自然科学基金资助项目(2017MS0835);内蒙古自治区科技计划项目(2017)

摘　　要：外伤性脑损伤(traumatic brain injuries,TBI)是指外力作用于颅骨所致的头皮、颅骨、硬脑膜和脑组织与外界相通,并由此引发脑组织一系列病理生理学改变的疾病。脑组织损伤后导致神经细胞缺血缺氧,脑血管通透性增加并引发一系列炎性细胞分泌增加,在促进炎症发生的同时改变多种细胞保护因子的表达,如低氧诱导因子-1(hypoxia-inducible-1,HIF-1)、葡萄糖转运蛋白-1(glucose transporter-1,GLUT-1)、小泛素样修饰蛋白-1(small ubiquitin-like modifier,SUMO-1)、CC趋化因子配体2(CC chemokines ligand 2,CCL2)、瞬时受体电位阳离子通道1(transient receptor potential channel 1,TRPC1)等蛋白质的表达产生一系列应激反应来应对缺氧,进而保护神经细胞免受进一步损伤。本文将围绕脑组织损伤后的神经细胞保护因子改变进行综述。TBI refers to the interaction of cranium,skull,dura and brain tissue caused by external force to the outside world,resulting in a series of pathophysiological changes of brain tissue.After brain injury leads to ischemia and hypoxia,cerebral vascular permeability and triggered a series of increased secretion of inflammatory cells,in promoting inflammation and change the expression of a variety of cell protective factors,such as hypoxia inducible factor-1（HIF-1）,glucose transporter-1（GLUT-1）,small ubiquitin like-1（SUMO-1）and CC chemokine ligand 2（CCL2）,transient receptor potential cation channel 1（TRPC1）expression protein to produce a series of stress responses to hypoxia,and protect nerve cells from further damage.This article will review the changes of nerve cell protective factors after brain tissue injury.

关 键 词：外伤性脑损伤 低氧诱导因子-1 葡萄糖转运蛋白-1 小泛素样修饰蛋白-1 CC趋化因子配体2 瞬时受体电位阳离子通道1 

分 类 号：R743.3[医药卫生—神经病学与精神病学]