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자료유형
학술저널
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대한신경과학회 Journal of Clinical Neurology Journal of Clinical Neurology 제10권 제2호
발행연도
2014.1
수록면
84 - 93 (10page)

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Background and Purpose Hypoxia, or ischemia, is a common cause of neurological deficits in the elderly. This study elucidated the mechanisms underlying ischemia-induced brain injury that results in neurological sequelae. Methods Cerebral ischemia was induced in male Sprague-Dawley rats by transient ligationof the left carotid artery followed by 60 min of hypoxia. A two-dimensional differential proteome analysis was performed using matrix-assisted laser desorption ionization-time-of-flightmass spectrometry to compare changes in protein expression on the lesioned side of the cortexrelative to that on the contralateral side at 0, 6, and 24 h after ischemia. Results The expressions of the following five proteins were up-regulated in the ipsilateralcortex at 24 h after ischemia-reperfusion injury compared to the contralateral (i.e., control)side: aconitase 2, neurotensin-related peptide, hypothetical protein XP-212759, 60-kDa heatshock protein, and aldolase A. The expression of one protein, dynamin-1, was up-regulatedonly at the 6-h time point. The level of 78-kDa glucose-regulated protein precursor on the lesioned side of the cerebral cortex was found to be high initially, but then down-regulated by 24 hafter the induction of ischemia-reperfusion injury. The expressions of several metabolic enzymes and translational factors were also perturbed soon after brain ischemia. Conclusions These findings provide insights into the mechanisms underlying the neurodegenerative events that occur following cerebral ischemia.

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