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Vol. 283, Issue 4, G957-G964, October 2002

Prevention of hepatic ischemia-reperfusion injury by green tea extract

Zhi Zhong^1,2, Matthias Froh², Henry D. Connor², Xiangli Li², Lars O. Conzelmann², Ronald P. Mason³, John J. Lemasters¹, and Ronald G. Thurman^2,

Departments of ¹ Cell and Developmental Biology and ² Pharmacology, University of North Carolina at Chapel Hill 27599; and ³ Laboratory Of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709

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 -(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-B and increased TNF- 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.

ischemia; free radicals; liver; nuclear factor-kappaB; cytokines

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Deceased 14 July 2001.

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