Protective effect of green tea polyphenol EGCG against neuronal damage and brain edema after unilateral cerebral ischemia in gerbils
Protective effect of green tea polyphenol EGCG against neuronal damage and brain edema after unilateral cerebral ischemia in gerbils
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DOI：
10.1002/jnr.20193
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发表时间：
2004-09-15
影响因子：
4.2
通讯作者：
Lee, SR
中科院分区：
文献类型：
--
作者：
Lee, H;Bae, JH;Lee, SR
先前的研究表明，绿茶多酚（-）-表没食子儿茶素没食子酸酯（EGCG）具有有效的自由基清除和抗氧化作用。谷氨酸会导致兴奋性毒性和氧化应激，这是脑缺血导致脑水肿和神经元损伤的重要病理生理反应。我们研究了 EGCG 对培养系统中兴奋性毒性神经元损伤的影响以及对沙鼠单侧脑缺血后脑水肿形成和病变的影响。在体外，通过与 N-甲基-D-天冬氨酸 (NMDA；10 μM)、AMPA (10 μM) 或红藻氨酸 (20 μM) 孵育 24 小时诱导兴奋性毒性。将EGCG（5μM）单独或与兴奋毒素一起添加到培养基中。我们检查了丙二醛 (MDA) 水平和神经元活力，以评估 EGCG 的效果。在体内，通过闭塞右侧颈总动脉30、60或90分钟，然后再灌注24小时来诱导单侧脑缺血。通过检查脑水肿、MDA 和梗塞来评估 EGCG 的保护作用。 EGCG（25 或 50 mg/kg，腹腔注射）注射两次，分别在缺血前 30 分钟和缺血后立即注射。 EGCG 减少培养系统中兴奋毒素诱导的 MDA 产生和神经元损伤。在体内研究中，用较低剂量的 EGCG 治疗沙鼠未能显示出神经保护作用；然而，较高的EGCG剂量减弱了脑缺血引起的MDA水平的增加。 EGCG还减少了缺血后脑水肿和梗塞体积的形成。这些结果表明，EGCG 未来可能有可能作为一种神经保护剂，对抗兴奋性毒性相关的神经系统疾病，例如脑缺血。 (C) 2004 Wiley-Liss, Inc.
Previous studies have demonstrated that a green tea polyphenol, (-)-epigallocatechine gallate (EGCG), has a potent free radical scavenging and antioxidant effect. Glutamate leads to excitotoxicity and oxidative stress, which are important pathophysiologic responses to cerebral ischemia resulting in brain edema and neuronal damage. We investigated the effect of EGCG on excitotoxic neuronal damage in a culture system and the effect on brain edema formation and lesion after unilateral cerebral ischemia in gerbils. In vitro, excitotoxicity was induced by 24-hr incubation with N-methyl-D-aspartate (NMDA; 10 muM), AMPA (10 muM), or kainate (20 muM). EGCG (5 muM) was added to the culture media alone or with excitotoxins. We examined malondialdehyde (MDA) level and neuronal viability to evaluate the effect of EGCG. In vivo, unilateral cerebral ischemia was induced by occlusion of the right common carotid artery for 30, 60, or 90 min and followed by reperfusion of 24 hr. Brain edema, MDA, and infarction were examined to evaluate the protective effect of EGCG. EGCG (25 or 50 mg/kg, intraperitoneally) was administered twice, at 30 min before and immediately after ischemia. EGCG reduced excitotoxin-induced MDA production and neuronal damage in the culture system. In the in vivo study, treatment of gerbils with the lower EGCG dose failed to show neuroprotective effects; however, the higher EGCG dose attenuated the increase in MDA level caused by cerebral ischemia. EGCG also reduced the formation of postischemic brain edema and infarct volume. These results demonstrate EGCG may have future possibilities as a neuroprotective agent against excitotoxicity-related neurologic disorders such as brain ischemia. (C) 2004 Wiley-Liss, Inc.