Department of Pharmacology, School of Basic Medical Sciences, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China.
Cell Mol Neurobiol. 2012 Mar;32(2):267-77. doi: 10.1007/s10571-011-9758-2. Epub 2011 Nov 11.
The function of Epigallocatechin gallate (EGCG), a main component of green tea, has been widely investigated, amelioration of synaptic transmission and neuroprotective effects against ischemia-induced brain damage among others. However, the mechanism underlying is still unveiled. We investigated the effects of EGCG on high frequency stimulation-induced long-term potentiation (LTP) in the Schaffer collateral-CA1 synapse with or without cerebral ischemia injury induced by middle cerebral artery occlusion (MCAO) in vivo to examine the possible relations between EGCG and synaptic transmission. Application of EGCG modulated synaptic transmission and produced a dose-dependent improvement of the induction of LTP. However, relative high-dose EGCG can block the induction of LTP at the Schaffer collateral-CA1 synapse in normal rat in vivo. In addition, the effects of EGCG were observed on the infarct volume and neurological deficit in rats subjected to MCAO; furthermore, the cell viability of primary cultured rat hippocampal and cortical neurons suffered from oxygen-glucose deprivation were evaluated with MTT and LDH assay, which showed significant neuroprotective properties in vitro. Surprisingly, the contents of the glutamate (Glu), glycine (Gly), and gamma-aminobutyric acid amino acids were totally disequilibrated before and after cerebral ischemia injury and could be rebalanced to original level by application of EGCG. Our results suggest that EGCG is able to improve the efficiency of synaptic transmission in cerebral ischemia injury with attenuated effect related to the neuroprotection of EGCG through regulating excitatory and inhibitory amino acid balance.
表没食子儿茶素没食子酸酯 (EGCG) 是绿茶的主要成分之一，其功能已得到广泛研究，包括改善突触传递和对缺血性脑损伤的神经保护作用等。然而，其作用机制仍未被揭示。我们研究了 EGCG 对体内大脑中动脉阻塞 (MCAO) 诱导的缺血损伤前后 Schaffer 侧枝-CA1 突触高频刺激诱导的长时程增强 (LTP) 的影响，以检查 EGCG 与突触传递之间的可能关系。EGCG 的应用调节了突触传递，并产生了剂量依赖性的 LTP 诱导改善。然而，在体内正常大鼠中，相对高剂量的 EGCG 可阻断 Schaffer 侧枝-CA1 突触的 LTP 诱导。此外，还观察了 EGCG 对 MCAO 大鼠梗死体积和神经功能缺损的影响；此外，还通过 MTT 和 LDH 测定评估了 EGCG 对氧葡萄糖剥夺培养的原代大鼠海马和皮质神经元细胞活力的影响，结果表明其具有显著的体外神经保护特性。令人惊讶的是，谷氨酸 (Glu)、甘氨酸 (Gly) 和γ-氨基丁酸氨基酸的含量在脑缺血损伤前后完全失衡，而应用 EGCG 可使其恢复到原始水平。我们的结果表明，EGCG 能够改善脑缺血损伤中的突触传递效率，其神经保护作用与调节兴奋性和抑制性氨基酸平衡有关。
