NGB Expression Changes After Ischemic Insult Of Brain Ischemic Preconditioning

Brain ischemic precondictioning(BIP) is a light cerebral ischemic stimulation to the animal nerve cell, which can induce endogenous protection in the brain and enhance the tolerance ability of brain tissue against following severe ischemic insult. The protection mechanism of BIP may have relationship with heat shock protein(HSP), adenosine, excitatory amino acids, original gene product, anti-apoptosis gene, and so on. But the certain mechanism remain unknown. In 2000, Burmester reported a newly identified protein-neuroglobin(NGB), which was a monomer globin with high oxygen affinity. Studies revealed high expressing NGB could do good to the neuron tolerance in hypoxia and diminish brain infarct size notably, which provided a new investigating path of protection mechanism of BIP. It is most unreality in clinic to prophylaxis and treat brain ischemic insult by BIP, but we can analysis NGB expressing changes of BIP and search for new opproach provocating similar responsive of BIP.Therefore, we lay out reformative focus-focus cerebral ischemia model, study NGB expressing changes in brain tissue and serum of BIP. Following experiments are performed.1. In matter of making focus BIP-focus cerebral ischemic damage model by MCAO, where the strand was plugged, whether external carotid artery(ECA) was deligated, there remained some arguement. In this study we observed smooth intromission could be obtained through common carotid artery (CCA), and remaining ECA unobstructed could decrease thrombus in internal carotid artery(ICA), which can prevent the difficulties of plugging bolt again. The animals had no obviously hemiplegia when they got consciousness after 10 min BIP of MCAO,24h later, ischemic damage was performed for 2h, then they all got contralateral hemiplegia.2. The NGB positive neurons in cerebral cortex had already been shown rising first and then descending during 72h period in 20min cerebral ischemic gerbil model, the summit reached at the moment of 24h. Our experiment demonstrated that the NGB positive neurons and NGB positive protein in contralateral cerebral cortex of BIP rat model stepped up gradually among 24h, then descending, but the positive neurons got peak at 16h in advance, the NGB positive protein and its integrated optical density got the peak at 24h. The positive neurons of BIP got summit at 16h, but the time was at 24h in ischemic insult merely, possibly it was due to BIP intervention. Moreover, NGB protein in 48h of all experimental BIP groups was expressed more than control group. Therefore, NGB might take action in the protection of BIP against brain ischemic insults.3. The experiment also indicated that NGB positive neurons in contralateral hippocampal CA1 and cells in hypothalamus aera grew in number more than control group. But peak moment emerge at 8h and 2h post ischemic insult respectively, they were both ahead than cerebral cortex. It might indicat hippocampal CA1 and hypothalamus aera were more sensitive against ischemic insult. The serum concentration of NGB in BIP groups was varing after ischemic insult, the amount of 48h increased much significangtly than 24h. The protection of BIP against ischemic damage might be reflected through the serum concentration of NGB.