L-alpha-glycerylphosphorylcholine reduces the microcirculatory dysfunction and nicotinamide adenine dinucleotide phosphate-oxidase type 4 induction after partial hepatic ischemia in rats

Background: We set out to investigate the microcirculatory consequences of hepatic ischemia-reperfusion (IR) injury and the effects of L-alpha-glycerylphosphorylcholine (GPC), a deacylated phospholipid derivative, on postischemic hepatocellular damage, with special emphasis on the expression of nico...

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Elmentve itt :
Bibliográfiai részletek
Szerzők: Hartmann Petra
Fet Ngwi
Garab Dénes
Szabó Andrea
Kaszaki József
Srinivasan Pramod Kadaba
Tolba René H.
Boros Mihály
Dokumentumtípus: Cikk
Megjelent: Academic Press 2014
Sorozat:JOURNAL OF SURGICAL RESEARCH 189 No. 1
doi:10.1016/j.jss.2013.12.025

mtmt:2573788
Online Access:http://publicatio.bibl.u-szeged.hu/11787
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245 1 0 |a L-alpha-glycerylphosphorylcholine reduces the microcirculatory dysfunction and nicotinamide adenine dinucleotide phosphate-oxidase type 4 induction after partial hepatic ischemia in rats  |h [elektronikus dokumentum] /  |c  Hartmann Petra 
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490 0 |a JOURNAL OF SURGICAL RESEARCH  |v 189 No. 1 
520 3 |a Background: We set out to investigate the microcirculatory consequences of hepatic ischemia-reperfusion (IR) injury and the effects of L-alpha-glycerylphosphorylcholine (GPC), a deacylated phospholipid derivative, on postischemic hepatocellular damage, with special emphasis on the expression of nicotinamide adenine dinucleotide phosphate oxidase type 4 (NOX4), which is predominantly expressed in hepatic microvessels. Materials and methods: Anesthetized male Sprague-Dawley rats were subjected to 60-min ischemia of the left liver lobes and 180-min reperfusion, with or without GPC treatment (50 mg/kg intravenously 5 min before reperfusion, n = 6 each). A third group (n = 6) served as saline-treated control. Noninvasive online examination of the hepatic microcirculation was performed hourly by means of modified spectrometry. Plasma tumor necrosis factor (TNF-α), high-mobility group box 1 protein (HMGB1), plasma aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase levels, tissue xanthine oxidoreductase (XOR) and myeloperoxidase (MPO) activities, and expressions of NOX2 and NOX4 proteins were determined. Results: Liver IR resulted in significant increases in NOX2 and NOX4 expressions and XOR and MPO activities, and approximately 2-fold increases in the levels of the inflammatory cytokines TNF-α and HMGB1. The microvascular blood flow and tissue oxygen saturation decreased by ∼20% from control values. GPC administration ameliorated the postischemic microcirculatory deterioration and reduced the liver necroenzyme levels significantly; the NOX4 expression, MPO activity, and HMGB1 level were also decreased, whereas the NOX2 expression, TNF-α level, and XOR activity were not influenced by GPC pretreatment. Conclusions: NOX4 activation is a decisive component in the IR-induced microcirculatory dysfunction. Exogenous GPC ameliorates the inflammatory activation, and preserves the postischemic microvascular perfusion and liver functions, these effects being associated with a reduced hepatic expression of NOX4. © 2014 Elsevier Inc. All rights reserved. 
700 0 1 |a Fet Ngwi  |e aut 
700 0 1 |a Garab Dénes  |e aut 
700 0 1 |a Szabó Andrea  |e aut 
700 0 1 |a Kaszaki József  |e aut 
700 0 1 |a Srinivasan Pramod Kadaba  |e aut 
700 0 1 |a Tolba René H.  |e aut 
700 0 1 |a Boros Mihály  |e aut 
856 4 0 |u http://publicatio.bibl.u-szeged.hu/11787/1/Hartmann_J_Surg_Surg_Res_2014_u.pdf  |z Dokumentum-elérés