Prevention of hepatic ischemia-reperfusion injury by green tea extract

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...

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Bibliographic Details
Published in:American journal of physiology: Gastrointestinal and liver physiology 2002-10, Vol.46 (4), p.G957-G964
Main Authors: ZHI ZHONG, FROH, Matthias, CONNOR, Henry D, XIANGLI LI, CONZELMANN, Lars O, MASON, Ronald P, LEMASTERS, John J, THURMAN, Ronald G
Format: Article
Language:English
Subjects:
Bile
Biological and medical sciences
Cytokines
Free radicals
Gastroenterology. Liver. Pancreas. Abdomen
Hemorrhage
Liver
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Medical sciences
Other diseases. Semiology
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Summary: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-kappaB 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.
ISSN:0193-1857
1522-1547