흥분독성 후 유발되는 지연성 신경세포 사멸 조절 유전자의 발굴 및 응용

초록

Brain damage following cerebral ischemia/reperfusion may be accentuated by postischemic events, which constitute the secondary injury processes. Of the many pathophysiological events that may contribute to secondary injury, cell-mediated processes in the postischemic inflammation and apoptosis have been extensively studied. Several lines of evidence suggest that there is an alteration of gene expression in the course of "delayed neuronal death". To identify such genes in rat brain following transient middle cerebral artery occlusion (MCAO), we carried out a series of experiments utilizing rat cDNA microarray. We focused on the changes of gene expression occurred from 12 hours to 4 days after MCAO in cerebral cortex and striatum of rat brain, wherein severe infarction occurred. Comparing the hybridization levels between ischemic and sham-operated animals revealed groups of genes, which were up- or down-regulated at each time point in postischemic brain. Extensive efforts to select and confirm the genes playing important roles in physiological context are undertaking. Subsequent functional studies of identified genes will provide a great opportunity to understand the mechanism underlying the delayed neuronal death in hypoxic ischemia.