Nagai Kaoru, Jiang Min Hai, Hada Junichi, Nagata Tetsu, Yajima Yukio, Yamamoto Satoshi, Nishizaki Tomoyuki
Department of Physiology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan.
Brain Res. 2002 Nov 29;956(2):319-22. doi: 10.1016/s0006-8993(02)03564-3.
The present study investigated the effects of (-)-epigallocatechin gallate (EGCG), which is the major component of polyphenol in green tea, on nitric oxide (NO) stress-induced neuronal damage, by monitoring NO mobilizations in the intact rat hippocampus and assaying the viability of cultured rat hippocampal neurons. A 10-min ischemia increased NO (NO(3)(-)/NO(2)(-)) concentrations in the intact rat hippocampus, while EGCG (50 mg/kg i.p.) inhibited the increase by 77% without affecting hippocampal blood flow. The NO donor, sodium nitroprusside (SNP; 50 microM), produced NO (NO(3)(-)/NO(2)(-)), while EGCG inhibited it in a dose-dependent manner at concentrations ranging from 50 to 200 microM. Treatment with SNP (100 microM) reduced the viability of cultured rat hippocampal neurons to 22% of control levels, while EGCG caused it to recover to 51% for 10 microM, 73% for 20 microM, and 70% for 50 microM. Taken together, it appears that EGCG could protect against ischemic neuronal damage by deoxidizing peroxynitrate/peroxynitrite, which is converted to NO radical or hydroxy radical.
本研究通过监测完整大鼠海马体中的一氧化氮（NO）释放情况以及检测培养的大鼠海马神经元的活力，研究了绿茶中多酚的主要成分（-）-表没食子儿茶素没食子酸酯（EGCG）对NO应激诱导的神经元损伤的影响。10分钟的局部缺血会增加完整大鼠海马体中的NO（NO₃⁻/NO₂⁻）浓度，而EGCG（50毫克/千克腹腔注射）可抑制这种增加，抑制率达77%，且不影响海马体的血流。NO供体硝普钠（SNP；50微摩尔）可产生NO（NO₃⁻/NO₂⁻），而EGCG在50至200微摩尔的浓度范围内以剂量依赖的方式抑制其产生。用SNP（100微摩尔）处理会使培养的大鼠海马神经元的活力降至对照水平的22%，而EGCG可使其恢复，10微摩尔时恢复到51%，20微摩尔时恢复到73%，50微摩尔时恢复到70%。综上所述，EGCG似乎可以通过还原过氧亚硝酸盐/过亚硝酸根来预防缺血性神经元损伤，过氧亚硝酸盐/过亚硝酸根可转化为NO自由基或羟基自由基。
