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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 cerebral cortex metabolite group and cerebral ischemic reperfusion time in stroke rats and to explore the molecular mechanism of cerebral cortical metabolism caused by ischemia-reperfusion injury. Methods Cerebral infarction model of middle cerebral artery occlusion (MCAO) was established in rats. The metabolomic group analysis technique based on nuclear magnetic resonance (NMR) was used to study the effects of MCAO on 3, 6, 24 h Changes in left cerebral cortex metabolite levels. Results After 3h ischemia-reperfusion in rats, there were some metabolic pathways such as insufficient energy, aggravated glycolysis and neurotransmitter disruption, and the above phenomenon was relieved at 6h after reperfusion. However, 24h perfusion, energy metabolism, anaerobic glycolysis, neurotransmitter metabolic disorders were aggravated. Conclusions Different degrees of reperfusion caused different degrees of cerebral cortical metabolic disorders, the results will help explore the pathological and molecular mechanisms of cerebral ischemia-reperfusion injury may provide clinical control of metabolic disorders at different time points after stroke Theoretical basis.