TY  - JOUR
IS  - 2
ID  - publicatio29032
Y1  - 2012///
UR  - https://doi.org/10.1097/SHK.0b013e31825d1ed0
N1  - Megjegyzés-23165531
N1 : Chemicals/CASnitric oxide, 10102-43-9; phosphatidylcholine, 55128-59-1, 8002-43-5; trinitrobenzenesulfonic acid, 16655-63-3, 2508-19-2; xanthine oxidase, 9002-17-9; Interleukin-6; Nitric Oxide, 10102-43-9; Peroxidase, 1.11.1.7; Phosphatidylcholines; Trinitrobenzenesulfonic Acid, 2508-19-2; Tumor Necrosis Factor-alpha; Xanthine Dehydrogenase, 1.17.1.4
Megjegyzés-23202014
N1 : Chemicals/CASnitric oxide, 10102-43-9; phosphatidylcholine, 55128-59-1, 8002-43-5; trinitrobenzenesulfonic acid, 16655-63-3, 2508-19-2; xanthine oxidase, 9002-17-9; Interleukin-6; Nitric Oxide, 10102-43-9; Peroxidase, 1.11.1.7; Phosphatidylcholines; Trinitrobenzenesulfonic Acid, 2508-19-2; Tumor Necrosis Factor-alpha; Xanthine Dehydrogenase, 1.17.1.4
Department of Paediatrics, Faculty of Medicine, University of Szeged, Szeged, Hungary            
            Institute of Surgical Research, Faculty of Medicine, University of Szeged, PO Box 427, Szeged H-6701, Hungary            
            Department of Pathology, Faculty of Medicine, University of Szeged, Szeged, Hungary            
            Cited By :12            
            Export Date: 8 February 2020            
            CODEN: SAGUA            
            Correspondence Address: Boros, M.; Institute of Surgical Research, Faculty of Medicine, University of Szeged, PO Box 427, Szeged H-6701, Hungary; email: boros.mihaly@med.u-szeged.hu            
            Chemicals/CAS: nitric oxide, 10102-43-9; phosphatidylcholine, 55128-59-1, 8002-43-5; trinitrobenzenesulfonic acid, 16655-63-3, 2508-19-2; xanthine oxidase, 9002-17-9; Interleukin-6; Nitric Oxide, 10102-43-9; Peroxidase, 1.11.1.7; Phosphatidylcholines; Trinitrobenzenesulfonic Acid, 2508-19-2; Tumor Necrosis Factor-alpha; Xanthine Dehydrogenase, 1.17.1.4
AV  - public
N2  - This study was designed to follow the time course of inflammatory activation in a rodent model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. We hypothesized that oral phosphatidylcholine (PC) pretreatment regimens may influence leukocyte-mediated microcirculatory reactions in this condition. In series I, Wistar rats were monitored 1 day after colitis induction (n = 24), and in series II (n = 24) on day 6 following a TNBS enema. The PC-pretreated animals received a 2% PC-enriched diet for 6 days before the TNBS enema (series I), or for 3 days before and 3 days after TNBS treatment (series II). The macrohemodynamics, serosal microcirculation (visualized by intravital videomicroscopy), colonic xanthine oxidoreductase, myeloperoxidase and nitric oxide end products, and changes in proinflammatory cytokine levels in plasma were measured. The mucosal structural injury was monitored in vivo by means of confocal laser scanning endomicroscopy. The TNBS enema induced a systemic hyperdynamic circulatory reaction with increased serosal capillary blood flow and significantly elevated colonic inflammatory enzyme activities, levels of nitric oxide production, and cytokine concentrations. Acute colitis caused disruption of the capillary network, whereas the morphologic damage was less severe in series II. The PC pretreatment protocols led to significant decreases in the serosal hyperemic reaction, the cytokine levels, and the inflammatory enzyme activities. The objective signs of tissue damage were reduced in both series, and the number of mucus-producing goblet cells in the resolving phase of colitis was increased. Dietary PC efficiently decreases the cytokine-mediated progression of inflammatory events and preserves the microvascular structure in the large intestine. Š 2012 by the Shock Society.
A1  -  Kovács Tamás
A1  -  Varga Gabriella
A1  -  Érces Dániel
A1  -  T?kés Tünde
A1  -  Tiszlavicz László
A1  -  Ghyczy Miklós
A1  -  Boros Mihály
A1  -  Kaszaki József
TI  - Dietary phosphatidylcholine supplementation attenuates inflammatory mucosal damage in a rat model of experimental colitis
SP  - 177
VL  - 38
SN  - 1073-2322
JF  - SHOCK
EP  - 185
ER  -