| Objective:To observe the change of NF-κB expression and cell apoptosis after hypoxic-ischemic brain damage(HIBD) in a neonatal rat model with HIBD.And the correlation between the post-HIBD and NF-κB(P65) expression and the role of NF-κB in the HIBD were also analyzed.Methods:Total of 128 SD rats,female or male,with the birth weight of 12 to 18 gram were randomly divided into 16 groups:sham operated group and ischemia/hypooxygen group. Both groups were then divided into 8 groups according to hypoxic ischemic time,including before treatment,2h group,6h group,12h group,18h group,24 h group,48h group and 72h group.All the rats in treatment group first suffered a right common carotid artery blotting and then been put into the hypoxic environment containing 8%O2 to induce hypoxic-ischemic brain damage.The brain tissue of each rat were then removed and immunohistochemistry staining of NF-κB,terminal-dexoy nucleotidyl transferase mediated nick end labeling(TUNEL) were performed.Results:After hypoxic ischemia and hypoxia,neonate rats have shown some abnormal behaviors of different extents.Under light microscope,we can also easily find brain edema and focal necrosis in neonate rat's brain after 2 to 6 hours of hypoxic-ischemia in the seven hypoxia and brain ischemic groups.Clearly infarct zone was found in brain of rats after 72 hours of hypoxic-ischemia.In blank control and sham control group,only very few NF-κB(P65) positive ceils and apoptosis cells in normal brain tissue was found.After hypoxia and ischemia,NF-κB (P65) positive cells were increased markedly,which can be find after 2 hours of hypoxic-ischemia,became obvious after 6 hours of hypoxic-ischemia,and reached its' peak after 24 hours of hypoxic-ischemia.Then,NF-κB(P65) positive cells begin to reduce after 24 to 72 hours of hypoxic-ischemia.NF-κB(P65) positive cells is still higher even after 72 hours of hypoxic-ischemia compared with the sham group.Two hours after hypoxic ischemia,the apoptosis cells can be found at cerebral cortex,increased significantly after 6 hours of hypoxic-ischemia,and extend to the peak at the 18th hour,then began to decrease gradually after 24 hours of hypoxic-ischemia,in which time the necrosis rather than the apoptosis has become the major type of cell death,and the necrosis became most severely during 48 to 72 hours after hypoxic ischemia.Conclusions:Within the first 24 hours after undergoing hypoxic-ischemic brain damage, apoptosis cells were gradually increased and at this time course,apoptosis is the major part of cell death,so it may be still reversible in the period.NF-κB(P65) expression was also increased in this time course and at this time.So the protein NF-κB(P65) may play a role in the apoptosis production in this stage.After 18h～24h of hypoxic-ischemia,apoptosis cells gradually decrease, necrosis has become the main style of brain cell death and in this period,the cell death is irreversible.NF-κB(P65) may induced necrosis in brain in this stage. |
