Induction of ischemic tolerance in rat liver via reduced nicotinamide adenine dinucleotide phosphate oxidase in Kupffer cells.

Induction of ischemic tolerance in rat liver via reduced nicotinamide adenine dinucleotide phosphate oxidase in Kupffer cells. Research Abstract Details 

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Induction of ischemic tolerance in rat liver via reduced nicotinamide adenine dinucleotide phosphate oxidase in Kupffer cells. Abstract Text:

Kazuaki Tejima,Masahiro Arai,Hitoshi Ikeda,Tomoaki Tomiya,Mikio Yanase,Yukiko Inoue,Takako Nishikawa,Naoko Watanabe,Natsuko Ohtomo,Masao Omata,Kenji Fujiwara,

AIM: To elucidate the mechanisms of hepatocyte preconditioning by H2O2 to better understand the pathophysiology of ischemic preconditioning. METHODS: The in vitro effect of H2O2 pretreatment was investigated in rat isolated hepatocytes subjected to anoxia/reoxygenation. Cell viability was assessed with propidium iodide fluorometry. In other experiments, rat livers were excised and subjected to warm ischemia/reperfusion in an isolated perfused liver system to determine leakage of liver enzymes. Preconditioning was performed by H2O2 perfusion, or by stopping the perfusion for 10 min followed by 10 min of reperfusion. To inhibit Kupffer cell function or reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, gadolinium chloride was injected prior to liver excision, or diphenyleneiodonium, an inhibitor of NADPH oxidase, was added to the perfusate, respectively. Histological detection of oxygen radical formation in Kupffer cells was performed by perfusion with nitro blue tetrazolium. RESULTS: Anoxia/reoxygenation decreased hepatocyte viability compared to the controls. Pretreatment with H2O2 did not improve such hepatocyte injury. In liver perfusion experiments, however, H2O2 preconditioning reduced warm ischemia/reperfusion injury, which was reversed by inhibition of Kupffer cell function or NADPH oxidase. Histological examination revealed that H2O2 preconditioning induced oxygen radical formation in Kupffer cells. NADPH oxidase inhibition also reversed hepatoprotection by ischemic preconditioning. CONCLUSION: H2O2 preconditioning protects hepatocytes against warm ischemia/reperfusion injury via NADPH oxidase in Kupffer cells, and not directly. NADPH oxidase also mediates hepatoprotection by ischemic preconditioning.

Induction of ischemic tolerance in rat liver via reduced nicotinamide adenine dinucleotide phosphate oxidase in Kupffer cells. Publishing Authors By Initials

K Tejima,M Arai,H Ikeda,T Tomiya,M Yanase,Y Inoue,T Nishikawa,N Watanabe,N Ohtomo,M Omata,K Fujiwara,

For similar cardiovascular diseases: vascular diseases: reperfusion injury research abstracts see: cardiovascular diseases: vascular diseases: reperfusion injury research

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Induction of ischemic tolerance in rat liver via reduced nicotinamide adenine dinucleotide phosphate oxidase in Kupffer cells. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: World journal of gastroenterology : WJG

VOLUME: 13

Page Numbers: 5071-8

Journal Abbreviation: World J. Gastroenterol.

ISSN: 1007-9327

DAY: 14

MONTH: Oct

YEAR: 2007

Induction of ischemic tolerance in rat liver via reduced nicotinamide adenine dinucleotide phosphate oxidase in Kupffer cells. Information

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LANGUAGE: eng

NlmUniqueID: 100883448

Induction of ischemic tolerance in rat liver via reduced nicotinamide adenine dinucleotide phosphate oxidase in Kupffer cells. Keywords Mesh Terms:

KEYWORDS: Reperfusion Injury

MESH TERMS: prevention & control

Chemical & Substance for Abstract: Induction of ischemic tolerance in rat liver via reduced nicotinamide adenine dinucleotide phosphate oxidase in Kupffer cells. Information

Substance Name: NADPH Oxidase

Registry Number: EC 1.6.3.1

Grant and Affiliation Information for Induction of ischemic tolerance in rat liver via reduced nicotinamide adenine dinucleotide phosphate oxidase in Kupffer cells.

AFFILIATION: Department of Gastroenterology, University of Tokyo, and Toshiba General Hospital, 6-3-22 Higashiooi, Shinagawa-ku, Tokyo 140-8522, Japan.

Country: China

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MEDLINETA: World J Gastroenterol

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