The NF-κB And Bcl-2 Expression And Neuron Apoptosis After Focal Cerebral Ischemia Reperfusion In Stroke-prone Renovascular Hypertensive Rats

Objective:To observe NF-κB and Bcl-2 expression and neuron apoptosis after focal cerebral ischemia reperfusion in Stroke-prone Renovascular Hypertensive Rats,exploring the effects of NF-κB and Bcl-2 on cell apoptosis.Methods:First the stroke-prone renovascular hypertensive rats(n=72)were made by two-kideney-two-clip method.After this operation,the rats were fed for two months,then was measured their blood pressure.Second they were subjected to middle cerebral artery occlusion(MCAO)and reperfusion injury of the brain.The hypertensive rats were randomly divided into seven groups:sham-operated control group,simple ischemia 2-hour group,3h,6h, 24h,48h,72h reperfusion after 2h of middle cerebral artery occlusion(MCAO)groups.Every group remained six rats at each time point after removing dead and unformed model ones.All rats wre executed,taken out brain and fixed at special time.The pathological changes was observed by HE staining.The NF-κB and Bcl-2 proteins were detected by immunohistochemistry staining methods and the cell apoptosis was also characterized by flow cytometry.Result:1,The blood pressure of the rats which were operated double renal artery stenosis was high.2,All the rats which were performed the operations of MCAO and reperfusion had right limb parelysis.3,NF-κB expressed on each time point.The most of NF-κB expression is on the point of 6 hour;the Bcl-2 positive neurons and the number of apoptotic cells in the cortex increased magnificently during 3 hours to 72 hours after reperfusion,peaked at 24h.Conclusion:Apoptosis is a pattern of neuron death after focal cerebral ischemia reperfusion in Stroke-prone Renovascular Hypertensive Rats;the NF -κB and Bcl-2 proteins are involved in the process of brain ischemia preperfusion injury;the expression time phases of NF -κB are 18h earlier than which of Bcl-2,and the change pattern of apoptotic cells was similar to that of Bcl-2 in the cortex;to intervene the activation of NF-κB and Bcl-2 in an appropriate time course may be a promising treatment.