The Relationships Between Expression Of NF-κB And Ncam And Neuronal Apoptosis After Cerebral Ischemia Reperfusions In Rats

Objective To observe NF-KB, NCAM expression and apoptosis after focal cerebralischemia reperfusion in rats, and explore the effects of NF-кB and NCAM on brain after damaged.Methods The model of focal ischemic reperfusion in SD Rats was induced by intraluminalmiddle cerebral artery (MCA) occlusion with a nylon monofilament suture. In situ hybridization was performed to examine the expression of NF-кBp65 mRAN and NCAM mRNA at 2,6,12h and l,2,3,7,14d after reperfusion and in shame-operated controls. Apoptosis was also characterized by terminal deoxynudeotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end-labeling (TUNEL) staining.Results In cortex and striatum, NF-кBp65 mRNA expression was detected fromreperfusion 2h, peaked at 1d, and decreased to normal level after 7d. TUNEL-positive cells were observed 2h after reperfusion in cortex and striatum, peaked at 2d ,ld after reperfusion respectively, while there was no remarkable change in sham-operated controls and ischemic hemisphere at 7d after reperfusion. NCAM mRNA expression was observed after reperfusion 2h in cortex and striatum, peaked at 12h, 1d respectively and was still higher at 7d.Conclusions The change of time-phase of cell apoptosis number is similar to that ofNF-KB in cortex and striatum after focal cerebral ischemia and reperfusion. So the expression of NF-кB can induce cell apoptosis and participate in the pathogenesis of cerebral ischemia and reperfusion injury. The increasing NCAM expression maybe an important factor of the neural plasticity in rats with ischemic brain injury.