Neuroglobin expression in rats after traumatic brain injury

• Published in: Neural regeneration research Vol. 7; no. 25; pp. 1960 - 1966
• Main Authors: Lin, Xin, Li, Min, Shang, Aijia, Hu, Yazhuo, Yang, Xiao, Ye, Ling, Bian, Suyan, Wang, Zhongfeng, Zhou, Dingbiao
• Format: Journal Article
• Language: English
• Published: India Medknow Publications & Media Pvt. Ltd 05.09.2012; Department of Surgery, Division of Nanlou, General Hospital of Chinese PLA, Beijing 100853, China%Department of Traumatic-Aesthetic Surgery, Huangsi Aesthetic Surgery Hospital, Beijing 100120, China%Department of Neurosurgery, Division of Surgery, General Hospital of Chinese PLA, Beijing 100853, China%Institute of Geriatrics, General Hospital of Chinese PLA, Beijing 100853, China%Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing 100071, China%Department of Cardiology, Division of Nanlou, General Hospital of Chinese PLA, Beijing 100853, China%Institute of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, China; Medknow Publications & Media Pvt Ltd
• Subjects: Apoptosis; Brain research; Cytoplasm; Cytotoxicity; Edema; Gene expression; Hypoxia; Ischemia; Neurosciences; Oxidative stress; Protein expression; Proteins; Research and Report : Brain Injury and Neural Regeneration; Surgery; Transgenic animals; Traumatic brain injury; 免疫组化染色; 创伤性脑损伤; 大鼠模型; 实时PCR; 神经细胞凋亡; 脑红蛋白; 蛋白表达; 颅脑损伤; Bcl-2; cerebral cortex; neural regeneration; Bax; neuron; traumatic brain injury; apoptosis; neuroglobin
• ISSN: 1673-5374; 1876-7958
• DOI: 10.3969/j.issn.1673-5374.2012.25.006

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.