The Expression Of The Cell-adhesion Molecules During Cerebral Ischemia-Reperfusion And The Relationship Between The Expression Of Adhesion Molecules And Inflammatory Response

ObjectiveThe cerebral ischemia-reperfusion may save cells from the borders of death, but may aggravate the cell damage even the cell death caused by the ischemia-reperfusion. The previous studies have shown that the excessive inflammatory reaction in the ischemic reperfusion of the brain is the main mechanisms of cerebral ischemic reperfusion injury. The inflammation response is the important pathological process to result in the cell injury and the secondary nerve cell destroy. In order to study the immunological mechanism of inflamatory injury mediated by the cell-adhesion molecules in cerebral ischemic reperfusion, we examined the relationship between inflammatory response and the expression of mRNA and protein of cell-adhesion molecules, ICAM-1,P-selection and E-selection.Methods(1) The animal models of middle cerebral artery occlusion (MCAO) were established with nelon threads in Wistar rats. The model group of rats were randomly divided into the five time points: 3h, 6h, 12h, 24h, 48h after reperfusion respectively and each time point include sham-operation group and model group.(2) Observe the pathology and morphology of ischemia-reperfusion injury by TTC staining, Hematoxylin-Eosin staining and electron microscope.(3) Observe the dynamic changes of the myelperoxidase activity of PMN by Enzyme assay technic.(4) mRNA and protein expression of cell-adhesion molecules ICAM-1, P-selection and E-selection during cerebral ischemia-reperfusion were examined by insitu hybridization and imunohistochemistry techniques respectively.(5) Image analysis was processed by computer picture analysis system.Results(1) The injury areas in MCAO were located in frontal parietal lobe cortex and striatum observed by TTC staining. The infarct area was peaked at 24h reperfusion and the infarct focus was already softened and necrosed at 48h time point of reperfusion.(2) The adhension and infiltration of neutrophils were found to begin at ischemia-6h reperfusion in cerebral cortex and striatum by HE staining, and became more and more serious with the process. At the same time, the necrosis center in inflammatory area magnified gradually.(3) MPO activity began to increas in the striatum and cortex 6h reperfusion and peaked at 48h post reperfusion.(4) mRNA expression of ICAM-1, P-selection and E-selection began to be detected at capillary endothelia cells in cerebral ischemic cortex and corpus striatumn 3h reperfusion and peaked at 6-12h of reperfusion. The protein expression of ICAM-1, P-selection and E-selection were coincident with that of mRNA expression in ischemic area by imunohistochemistry assay. However, the peak point was extended and reached at 24h reperfusion.ConclusionsBoth of the mRNA and protein expression of ICAM-1, P-selection and E-selection were upregulated after cerebral ischemia-reperfusion, which boosted the inflammatory cascade response that mediated by the cell-adhesive molecules.