Neuroglobin expression in rats after traumatic brain injury  

作　　者：Xin Lin Min Li Aijia Shang Yazhuo HU Xiao Yang Ling Ye Suyan Bian ZhongfengWang Dingbiao Zhou 

机构地区：[1]Department of Surgery, Division of Nanlou, General Hospital of Chinese PLA, Beijing 100853, China [2]Department of Traumatic-Aesthetic Surgery, Huangsi Aesthetic Surgery Hospital, Beijing 100120, China [3]Department of Neurosurgery, Division of Surgery, General Hospital of Chinese PLA, Beijing 100853, China [4]Institute of Geriatrics, General Hospital of Chinese PLA, Beijing 100853, China [5]Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing 100071, China [6]Department of Cardiology, Division of Nanlou, General Hospital of Chinese PLA, Beijing 100853, China [7]Institute of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, China

出　　处：《Neural Regeneration Research》2012年第25期1960-1966,共7页中国神经再生研究（英文版）

基　　金：supported by General Program of National Natural Science Foundation of China,No. 30400465,30571903;Open Project from Medical Neurobiology of State Key Laboratory (09-08) of Fudan University

摘　　要：In this study, we used a rat model of severe closed traumatic brain injury to explore the relationship between neuroglobin, brain injury and neuronal apoptosis. Real-time PCR showed that neuroglobin mRNA expression rapidly increased in the rat cerebral cortex, and peaked at 30 minutes and 48 hours following traumatic brain injury. Immunohistochemical staining demonstrated that neuroglobin expression increased and remained high 2 hours to 5 days following injury. The rate of increase in the apoptosis-related Bax/Bcl-2 ratio greatly decreased between 30 minutes and 1 hour as well as between 48 and 72 hours post injury. Expression of neuroglobin and the anti-apoptotic factor Bcl-2 greatly increased, while that of the proapoptotic factor decreased, in the cerebral cortex post severe closed traumatic brain injury. It suggests that neuroglobin might protect neurons from apoptosis after traumatic injury by regulating Bax/Bcl-2 pathway.In this study, we used a rat model of severe closed traumatic brain injury to explore the relationship between neuroglobin, brain injury and neuronal apoptosis. Real-time PCR showed that neuroglobin mRNA expression rapidly increased in the rat cerebral cortex, and peaked at 30 minutes and 48 hours following traumatic brain injury. Immunohistochemical staining demonstrated that neuroglobin expression increased and remained high 2 hours to 5 days following injury. The rate of increase in the apoptosis-related Bax/Bcl-2 ratio greatly decreased between 30 minutes and 1 hour as well as between 48 and 72 hours post injury. Expression of neuroglobin and the anti-apoptotic factor Bcl-2 greatly increased, while that of the proapoptotic factor decreased, in the cerebral cortex post severe closed traumatic brain injury. It suggests that neuroglobin might protect neurons from apoptosis after traumatic injury by regulating Bax/Bcl-2 pathway.

关 键 词：NEUROGLOBIN traumatic brain injury NEURON APOPTOSIS cerebral cortex BAX Bcl-2 neuralregeneration 

分 类 号：Q78[生物学—分子生物学] F407.7[经济管理—产业经济]