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Am J Physiol Gastrointest Liver Physiol (June 12, 2002). doi:10.1152/ajpgi.00216.2001
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Articles in PresS, published online ahead of print June 12, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00216.2001
Submitted on May 22, 2001
Accepted on June 5, 2002

Prevention of Hepatic Ischemia-Reperfusion Injury by Green Tea Extract

Zhi Zhong1*, Matthias Froh2, Henry D Connor3, Xiangli Li2, Lars O Conzelmann2, Ronald P Mason4, John J Lemasters5, and Ronald G Thurman2

1 Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, NC, USA; Department of Pharmacology, University of North Carolina, Chapel Hill, NC, USA
2 Department of Pharmacology, University of North Carolina, Chapel Hill, NC, USA
3 Department of Pharmacology, University of North Carolina, Chapel Hill, NC, USA; Laboratory of Pharmacology and Chemistry, NIEHS, RTP, NC, USA
4 Laboratory of Pharmacology and Chemistry, NIEHS, RTP, NC, USA
5 Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, NC, USA

* To whom correspondence should be addressed. E-mail: zzhong{at}med.unc.edu.

These experiments were designed to determine if green tea extract (GTE), which contains polyphenolic free radical scavengers, would prevent hypoxia/reperfusion injury in the liver. Rats were fed a powdered diet containing 0-0.3% GTE starting 5 days prior to 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 ESR. Ischemia/reperfusion increases transaminase release and causes pathological changes including focal necrosis and 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 POBN/radical adducts nearly 2-fold, 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 as well as myeloperoxidase activity. These effects were all blocked by GTE. Taken together, these results demonstrate that GTE scavenges free radicals in the liver after ischemia/reoxygenation thus preventing formation of toxic cytokines. Therefore, GTE could prove to be effective in decreasing hepatic injury in disease states where ischemia/reperfusion occurs.




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