The Effect Of Chronic Intermittent Hypoxia On NF-κB,ICAM-1,TNF-α Expressions In Cortex Of Cerebral Ischemia Reperfusion Injury Rats

ObjectiveTo study the roles of chronic intermittent hypoxia,or combined with cerebral ischemia reperfusion injury in the expression of nuclear factor-κB p56,intercellular adhesion molecule-1 and tumor necrosis factor-αof brain cortex in Rats.Methods In this experiment,36 Sprague-Dewley rats were randomly divided into 4groups,which were control group,CIH group,CIR group,CIH+CIR group.The chronic intermittent hypoxia model was made,and then the rats were exposed to cerebral ischemia reperfusion injury.The expression of NF-κB p65,ICAM-1 and TNF-αin brain cortex were detected by immunohistochemistry.The effusion of polymorphonuclear leucocytes in brain tissue was detected by HE staining. Infarct size was also investigated by TTC staining.ResultsGroup CIH+CIR,contrasting to group CIR,the Longas score were higher(P<0.05) ; the infarct size were bigger(P<0.001). Chronic intermittent hypoxia make the expression of NF-κB p65,ICAM-1 and TNF-αin cortex of rats increase,as well as cerebral ischemia reperfusion injury. Moreover,there was an interactive effect between chronic intermmittent hypoxia and cerebral ischemia reperfusion (all P<0.05).In addition,a positive correlation (all P<0.05) was observed between the expression of NF-κB p65 and the expression of ICAM-1,as well as between NF-κB p65 and TNF-α.ConclusionChronic intermittent hypoxia may increased imflammation response in rats and its probable mechanism involves the increased expression of NF-κB p65,ICAM-1 and TNF-αof cortex .