Prevention of hepatic ischemia-reperfusion injury by green tea extract

Prevention of hepatic ischemia-reperfusion injury by green tea extract Abstract 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 α-(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-κB and increased TNF-α 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 Footnotes ↵ † Deceased 14 July 2001. This study was supported, in part, by National Institutes of Health grants. Present address for H. Connor: Dept. of Chemistry, Kentucky Wesleyan College, Owensboro, KY 42301. Address for reprint requests and other correspondence: Z. Zhong, Dept. of Cell and Developmental Biology, CB# 7090, Univ. of North Carolina at Chapel Hill, Chapel Hill, NC 27599. The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. June 12, 2002;10.1152/ajpgi.00216.2001 Copyright © 2002 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Gastrointestinal and Liver Physiology The American Physiological Society

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0193-1857
eISSN
1522-1547
DOI
10.1152/ajpgi.00216.2001
Publisher site
See Article on Publisher Site

Abstract

Abstract 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 α-(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-κB and increased TNF-α 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 Footnotes ↵ † Deceased 14 July 2001. This study was supported, in part, by National Institutes of Health grants. Present address for H. Connor: Dept. of Chemistry, Kentucky Wesleyan College, Owensboro, KY 42301. Address for reprint requests and other correspondence: Z. Zhong, Dept. of Cell and Developmental Biology, CB# 7090, Univ. of North Carolina at Chapel Hill, Chapel Hill, NC 27599. The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. June 12, 2002;10.1152/ajpgi.00216.2001 Copyright © 2002 the American Physiological Society

Journal

AJP - Gastrointestinal and Liver PhysiologyThe American Physiological Society

Published: Oct 1, 2002

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