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Objective: To evaluate the expression of NF-κB and Doublecortin incerebral ischemic preconditioning, and to investigate the effect of NF-κB and Doublecortin in mediating ischemic toleran by Ischemic preconditioning.Methods:A total of fifty-four Wistar male rats (6 - week - old) were randomly assigned into 3 groups as follows: 24 hours group, 48 hours group and 72 hours group (n = 18 in each group). Then the each group randomly assigned to3 groups again: pMCAO group (group R ), pMCAO after preconditioning group(group IPR ), sham- operation(group S ),(n = 6 in each group). Rats in group IPR were first infused saline solution into the left internal carotid artery to establish a Ischemic preconditioning model.After three days,a focal cerebral ischemia model was induced by middle cerebral artery intraluminal suture occlusion (MCAO) method with group R at the same time.Rats in group S were only isolated carotid artery. In the corresponding time points after surgery,rats were observed Neurological deficits according to the Longas score and detected the expressions of NF-κB mRNA , Doublecortin mRNA assessed by real - time quantitative PCR.Results:(1) the Neurological deficits score in group IPR is less than that in group R at any time(P<0.05).(2) Compared with the group S, at the same point of time ,the expressions of NF-κB mRNA , Doublecortin mRNA in group R brain was significantly increased,and the longer time of the more(P<0.05)(3)Compared with the group R, at the same point of time, the expressions of NF-κB mRNA ,but Doublecortin mRNA in group IPR was raised remarkably.Conclusion: Brain ischemia may active the NF-κB signaling pathways and Neural stem cells . Ischemic preconditioning could induce ischemic tolerance.The negative regulation of NF-κB signaling pathways and improving the expression of Neural Precursor Cell may be the major mechanism of neuroprotective effect .
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