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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| Dokumentumtípus: | Cikk |
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Academic Press
2014
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| 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 |
| LEADER | 03197nab a2200289 i 4500 | ||
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| 005 | 20200221112955.0 | ||
| 008 | 170721s2014 hu o 0|| zxx d | ||
| 022 | |a 0022-4804 | ||
| 024 | 7 | |a 10.1016/j.jss.2013.12.025 |2 doi | |
| 024 | 7 | |a 2573788 |2 mtmt | |
| 040 | |a SZTE Publicatio Repozitórium |b hun | ||
| 041 | |a zxx | ||
| 100 | 1 | |a Hartmann Petra | |
| 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 |
| 260 | |a Academic Press |c 2014 | ||
| 300 | |a 32-40 | ||
| 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 |