详细信息
基于核磁共振技术研究脑缺血再灌注大鼠脑皮质代谢物组水平变化的分子机制
Molecular mechanism of metabolic changes in rat cerebral cortex after cerebral ischemia-reperfusion:an NMR-based study
文献类型:期刊文献
中文题名:基于核磁共振技术研究脑缺血再灌注大鼠脑皮质代谢物组水平变化的分子机制
英文题名:Molecular mechanism of metabolic changes in rat cerebral cortex after cerebral ischemia-reperfusion:an NMR-based study
作者:马夏珍[1];张天舒[1];阮志[2];黄瑾[1];张乃霞[3];刘霞[3]
机构:[1]华东理工大学药学院上海市新药筛选重点实验室,上海200237;[2]中国科学院上海药物研究所受体结构与功能重点实验室,上海201203;[3]中国科学院上海药物研究所分析化学研究室,上海201203
年份:2016
卷号:37
期号:11
起止页码:1338
中文期刊名:第二军医大学学报
外文期刊名:Academic Journal of Second Military Medical University
收录:CSTPCD;;Scopus;北大核心:【北大核心2014】;CSCD:【CSCD2015_2016】;
基金:国家自然科学基金(21272246);国家重点基础研究发展计划("973"计划;2013CB910900)~~
语种:中文
中文关键词:核磁共振;卒中;脑缺血;再灌注损伤;代谢紊乱;分子机制
外文关键词:nuclear magnetic resonance; stroke; brain ischemia; reperfusion injuries; metabolic disorders; molecular mechanism
摘要:目的研究脑卒中大鼠脑皮质代谢物组水平与脑缺血再灌注时间的关系,探讨缺血再灌注损伤导致的脑皮质代谢紊乱的分子机制。方法采用大脑中动脉闭塞法(MCAO)制备大鼠局灶性左脑缺血的脑卒中模型,运用基于核磁共振的代谢物组分析技术,研究MCAO大鼠脑缺血再灌注3、6、24h时左脑皮质代谢物水平变化。结果大鼠左脑皮质缺血再灌注3h时出现能量不足、糖酵解加剧、神经递质紊乱等代谢途径的改变,再灌注6h时因机体自身调节作用,上述现象均有所缓解;然而再灌注24h时,能量代谢、无氧酵解、神经递质代谢紊乱等均加重。结论再灌注不同时间点引起了不同程度的大脑皮质代谢紊乱,该结果将有助于探索脑缺血再灌注损伤的病理分子机制,可为临床上调控脑卒中发生后不同时间点的代谢紊乱提供理论基础。
Objective To investigate the relationship between metabolite levels and the time of cerebral ischemia-reperfusion in the left cortex of rats, so as to explore the molecular mechanism of cortical metabolic disorders induced by ischemia-reperfusion injury. Methods Stroke models of focal cerebral ischemia in rats were established by middle cerebral artery occlusion (MCAO). Then a nuclear magnetic resonance (NMR)-based metabolome analytical approach was carried out to analyze the metabolite levels in the left cortex of MCAO rats at different time points (3, 6, and 24 h) after reperfusion. Results Some changes of metabolic pathways, such as energy deficiency, glycolysis aggravation, and neurotransmitter disorders, were observed in the left cortex of MCAO rats at 3 h after reperfusion. All the above-mentioned disorders were alleviated by the autoregulation at 6 h after reperfusion. However, the forementioned metabolic disturbances became severe after 24-hour reperfusion. Conclusion Our results suggest that different extents of metabolic disturbance appears in the cortex at different time points after reperfusion, which might help to understand the molecular mechanism of cerebral ischemia-reperfusion injury, providing reference for regulating metabolic disorders at different time points after stroke in clinic.
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