Alvarez E, Leiro J, Orallo F
Departamento de Farmacología, Facultad de Farmacia, Universidad de Santiago de Compostela, Spain.
Int Immunopharmacol. 2002 May;2(6):849-55. doi: 10.1016/s1567-5769(02)00032-2.
The toxic effects derived from overproduction of oxygen radicals [reactive oxygen species (ROS)] by immune cells can be partially abolished by the antioxidant activities of plant polyphenols. In the present study, we investigated the antioxidant action of a catechin, (-)-epigallocatechin-3-gallate (EGCG), on the respiratory-burst responses of rat peritoneal macrophages. EGCG at concentrations of 50-200 microM blocked the production of nitric oxide by macrophages stimulated in vivo with sodium thioglycollate then 5 days later in vitro with lipopolysaccharide and gamma-interferon. At 1-100 microM, EGCG also inhibited the extracellular liberation of oxygen radicals by resident peritoneal macrophages stimulated with the protein kinase C activator phorbol 12-myristate 13-acetate (PMA). At low concentrations (1-5 microM), EGCG increased the reduction of nitro blue tetrazolium (NBT) by the superoxide anions generated in the non-enzymatic system NADH/PMS, acting as a pro-oxidant agent, while at concentrations above 10 microM, EGCG acts as a scavenger of superoxide anions. These results show that EGCG is capable of modulating ROS production during the respiratory burst of rat peritoneal macrophages by acting as a superoxide anion scavenger. EGCG may therefore be useful in the prevention and treatment of diseases due to increased free radical production.
免疫细胞过度产生氧自由基[活性氧（ROS）]所产生的毒性作用，可被植物多酚的抗氧化活性部分消除。在本研究中，我们研究了一种儿茶素，（-）-表没食子儿茶素-3-没食子酸酯（EGCG），对大鼠腹腔巨噬细胞呼吸爆发反应的抗氧化作用。浓度为50-200微摩尔的EGCG可阻断巨噬细胞一氧化氮的产生，这些巨噬细胞先用巯基乙酸钠在体内刺激，然后在5天后用脂多糖和γ-干扰素在体外刺激。在1-100微摩尔浓度下，EGCG还可抑制蛋白激酶C激活剂佛波酯12-肉豆蔻酸酯13-乙酸酯（PMA）刺激的驻留腹腔巨噬细胞释放细胞外氧自由基。在低浓度（1-5微摩尔）时，EGCG可增加非酶系统NADH/PMS产生的超氧阴离子对硝基蓝四唑（NBT）的还原作用，此时EGCG作为促氧化剂，而在浓度高于10微摩尔时，EGCG则作为超氧阴离子清除剂。这些结果表明，EGCG能够通过作为超氧阴离子清除剂来调节大鼠腹腔巨噬细胞呼吸爆发期间的ROS产生。因此，EGCG可能有助于预防和治疗因自由基产生增加而导致的疾病。
