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.