Lee S, Suh S, Kim S
Department of Pharmacology, School of Medicine, Keimyung University, Taegu, South Korea.
Neurosci Lett. 2000 Jun 30;287(3):191-4. doi: 10.1016/s0304-3940(00)01159-9.
Recent studies have shown that green tea polyphenols reduce free radical-induced lipid peroxidation. Oxygen free radical injury plays an important role in neuronal damage induced by brain ischemia and reperfusion. The purpose of this study was to examine whether (-)-epigallocatechin gallate (EGCG) would reduce neuronal damage after transient global ischemia in the gerbils because EGCG has a potent antioxidant property as a green tea polyphenol. To produce transient global ischemia, both common carotid arteries were occluded for 3 min with microaneurysmal clips. The gerbils were treated with EGCG (10, 25, or 50 mg/kg, i.p.) immediately after ischemia. Neuronal cell damage in the hippocampal CA1 region was evaluated quantitatively 5 days after ischemia by a blinded investigator. EGCG at the dose of 10 mg/kg failed to reduce hippocampal neuronal damage. However, EGCG when administered at the dose of 25 or 50 mg/kg significantly reduced hippocampal neuronal damage in a dose-dependent manner (P<0.001, respectively). The present results show that the green tea polyphenol, EGCG, has a neuroprotective effect against neuronal damage following global ischemia in the gerbils.
最近的研究表明,绿茶多酚可减少自由基诱导的脂质过氧化。氧自由基损伤在脑缺血再灌注诱导的神经元损伤中起重要作用。本研究的目的是检验(-)-表没食子儿茶素没食子酸酯(EGCG)是否会减少沙鼠短暂性全脑缺血后的神经元损伤,因为EGCG作为一种绿茶多酚具有强大的抗氧化特性。为产生短暂性全脑缺血,用微动脉瘤夹将双侧颈总动脉夹闭3分钟。沙鼠在缺血后立即接受EGCG(10、25或50mg/kg,腹腔注射)治疗。缺血5天后,由一位不知情的研究者对海马CA1区的神经元细胞损伤进行定量评估。10mg/kg剂量的EGCG未能减少海马神经元损伤。然而,25或50mg/kg剂量的EGCG以剂量依赖方式显著减少了海马神经元损伤(分别为P<0.001)。目前的结果表明,绿茶多酚EGCG对沙鼠全脑缺血后的神经元损伤具有神经保护作用。