Prevention of hepatic ischemia-reperfusion injury by green tea extract.
Prevention of hepatic ischemia-reperfusion injury by green tea extract.
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DOI：
10.1152/ajpgi.00216.2001
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发表时间：
2002-10
期刊：
影响因子：
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通讯作者：
Z. Zhong;M. Froh;H. Connor;Xiangli Li;L. Conzelmann;R. Mason;J. Lemasters;R. Thurman
中科院分区：
文献类型：
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作者：
Z. Zhong;M. Froh;H. Connor;Xiangli Li;L. Conzelmann;R. Mason;J. Lemasters;R. Thurman
这些实验旨在确定绿茶提取物（GTE）是否含有多酚自由基清除剂，以防止肝脏缺血再灌注损伤。大鼠在肝热缺血再灌注前5天开始饲喂含0-0.3% GTE的粉末状饲料。用自旋捕获试剂α -（4-吡啶-1-氧化物）- n-叔丁基硝基酮（4-POBN）捕获胆汁中的自由基，并用电子自旋共振谱法测定。肝缺血再灌注增加转氨酶释放，引起肝局灶性坏死、肝内白细胞浸润等病理改变。转氨酶释放减少85%以上，0.1% GTE几乎完全阻断病理变化。缺血-再灌注使胆汁中的4-POBN/自由基加合物增加近两倍，GTE在很大程度上阻断了这一作用。表儿茶素是一种主要的绿茶多酚，具有与GTE相似的保护作用。此外，肝缺血再灌注激活NF-kappa B，增加tnf - α mRNA和蛋白的表达。这些效应都被GTE阻断了。综上所述，这些结果表明，GTE清除缺血氧化后肝脏中的自由基，从而防止有毒细胞因子的形成。因此，GTE可以证明在发生缺血-再灌注的疾病状态下有效减轻肝损伤。
These experiments were designed to determine whether green tea extract (GTE), which contains polyphenolic free radical scavengers, prevents ischemia-reperfusion injury to the liver. Rats were fed a powdered diet containing 0-0.3% GTE starting 5 days before hepatic warm ischemia and reperfusion. Free radicals in bile were trapped with the spin-trapping reagent alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (4-POBN) and measured using electron spin resonance spectroscopy. Hepatic ischemia-reperfusion increased transaminase release and caused pathological changes including focal necrosis and hepatic leukocyte infiltration in the liver. Transaminase release was diminished by over 85% and pathological changes were almost totally blocked by 0.1% dietary GTE. Ischemia-reperfusion increased 4-POBN/radical adducts in bile nearly twofold, an effect largely blocked by GTE. Epicatechin, one of the major green tea polyphenols, gave similar protection as GTE. In addition, hepatic ischemia-reperfusion activated NF-kappa B and increased TNF-alpha mRNA and protein expression. These effects were all blocked by GTE. Taken together, these results demonstrate that GTE scavenges free radicals in the liver after ischemiareoxygenation, thus preventing formation of toxic cytokines. Therefore, GTE could prove to be effective in decreasing hepatic injury in disease states where ischemia-reperfusion occurs.