Muranyi Marianna, Li Ping-An
Department of Cell, John A. Burns School of Medicine, University of Hawaii at Manoa, 1960 East-West Road, Biomedical Tower T514, Honolulu, HI 96822, USA.
Neurosci Lett. 2006 Jan 30;393(2-3):119-21. doi: 10.1016/j.neulet.2005.09.079. Epub 2005 Oct 27.
Transient global cerebral ischemia results in selective neuronal death in the vulnerable hippocampal CA1 pyramidal neurons in a delayed manner. Hyperglycemia accelerates and exacerbates neuronal damage in this region. The object of this study was to determine whether hyperglycemia-enhanced damage is associated with increased production of superoxide anion after ischemia. The results showed that hyperglycemic ischemia caused a significant increase of superoxide production in the hippocampal CA1 neurons compared to normoglycemic animals after 18 h of recirculation, suggesting that enhanced superoxide anion production may mediate the hyperglycemia-accelerated and -enhanced neuronal death in the hippocampal CA1 area after ischemia and reperfusion.
短暂性全脑缺血会导致易损的海马CA1锥体神经元选择性延迟性死亡。高血糖会加速并加剧该区域的神经元损伤。本研究的目的是确定高血糖增强的损伤是否与缺血后超氧阴离子生成增加有关。结果表明,与血糖正常的动物相比,在再灌注18小时后,高血糖缺血导致海马CA1神经元中超氧生成显著增加,这表明超氧阴离子生成增强可能介导了缺血再灌注后海马CA1区高血糖加速和增强的神经元死亡。