Kato N, Yanaka K, Nagase S, Hirayama A, Nose T
Department of Neurosurgery, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan.
Acta Neurochir (Wien). 2003 Jun;145(6):489-93; discussion 493. doi: 10.1007/s00701-003-0036-z.
Cerebral ischaemia-reperfusion injury is associated with the generation of reactive oxygen species during the early phases of reoxygenation. EPC-K1, a phosphate diester of vitamins C and E, has been reported to possess potent hydroxyl radical scavenging activity. This study was performed to investigate the effectiveness of EPC-K1 in attenuating cerebral ischaemia-reperfusion injury in a rat model of transient focal cerebral ischaemia.
We evaluated the efficacy of EPC-K1 by measuring the concentration of cerebral thiobarbituric acid reactive substances (TBARS), an indicator of the extent of lipid peroxidation by free radicals, and infarct size in rats subjected to one hour of cerebral ischaemia and 4, 24, or 72 hours of reperfusion.
EPC-K1 significantly reduced both the cerebral TBARS level and the infarct size in a rat model of transient focal cerebral ischaemia. These results indicate that EPC-K1 administration during the early stages of reperfusion ameliorates ischaemic brain injury by inhibiting lipid peroxidation.
This report is the first to describe the protective mechanism of EPC-K1 by measuring both the TBARS level and infarct size in a rat model of transient focal cerebral ischaemia, and may suggest a potential clinical approach for the treatment of ischaemic cerebrovascular disease.
脑缺血再灌注损伤与复氧早期活性氧的产生有关。据报道，维生素C和E的磷酸二酯EPC-K1具有强大的羟自由基清除活性。本研究旨在探讨EPC-K1在短暂性局灶性脑缺血大鼠模型中减轻脑缺血再灌注损伤的有效性。
我们通过测量脑硫代巴比妥酸反应性物质（TBARS）的浓度（自由基脂质过氧化程度的指标）以及经历1小时脑缺血和4、24或72小时再灌注的大鼠的梗死面积，来评估EPC-K1的疗效。
在短暂性局灶性脑缺血大鼠模型中，EPC-K1显著降低了脑TBARS水平和梗死面积。这些结果表明，在再灌注早期给予EPC-K1可通过抑制脂质过氧化来改善缺血性脑损伤。
本报告首次通过测量短暂性局灶性脑缺血大鼠模型中的TBARS水平和梗死面积来描述EPC-K1的保护机制，并可能为缺血性脑血管疾病的治疗提供一种潜在的临床方法。
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