title: Protective effects of L-alpha-glycerylphosphorylcholine on ischaemia-reperfusion-induced inflammatory reactions.
abstract: OBJECTIVE
  Choline-containing dietary phospholipids, including phosphatidylcholine (PC), may function as anti-inflammatory substances, but the mechanism remains largely unknown. We investigated the effects of L-alpha-glycerylphosphorylcholine (GPC), a deacylated PC derivative, in a rodent model of small intestinal ischaemia-reperfusion (IR) injury.
  
  
  METHODS
  Anaesthetized Sprague-Dawley rats were divided into control, mesenteric IR (45 min mesenteric artery occlusion, followed by 180 min reperfusion), IR with GPC pretreatment (16.56 mg kg⁻¹ GPC i.v., 5 min prior to ischaemia) or IR with GPC post-treatment (16.56 mg kg⁻¹ GPC i.v., 5 min prior to reperfusion) groups. Macrohaemodynamics and microhaemodynamic parameters were measured; intestinal inflammatory markers (xanthine oxidoreductase activity, superoxide and nitrotyrosine levels) and liver ATP contents were determined.
  
  
  RESULTS
  The IR challenge reduced the intestinal intramural red blood cell velocity, increased the mesenteric vascular resistance, the tissue xanthine oxidoreductase activity, the superoxide production, and the nitrotyrosine levels, and the ATP content of the liver was decreased. Exogenous GPC attenuated the macro- and microcirculatory dysfunction and provided significant protection against the radical production resulting from the IR stress. The GPC pretreatment alleviated the hepatic ATP depletion, the reductions in the mean arterial pressure and superior mesenteric artery flow, and similarly to the post-treatments with GPC, also decreased the xanthine oxidoreductase activity, the intestinal superoxide production, the nitrotyrosine level, and normalized the microcirculatory dysfunction.
  
  
  CONCLUSIONS
  These data demonstrate the effectiveness of GPC therapies and provide indirect evidence that the anti-inflammatory effects of PC could be linked to a reaction involving the polar part of the molecule.
authors.affiliation: Institute of Surgical Research, University of Szeged, Pécsi u. 6., Szeged, 6720, Hungary.
authors.forename: Tünde
authors.initials: T
authors.lastname: Tőkés
authors.forename: Eszter
authors.initials: E
authors.lastname: Tuboly
authors.forename: Gabriella
authors.initials: G
authors.lastname: Varga
authors.forename: László
authors.initials: L
authors.lastname: Major
authors.forename: Miklós
authors.initials: M
authors.lastname: Ghyczy
authors.forename: József
authors.initials: J
authors.lastname: Kaszaki
authors.forename: Mihály
authors.initials: M
authors.lastname: Boros
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000627:therapeutic use*; D019587:Dietary Supplements; D004195:Disease Models, Animal; D004751:Enteritis / Q000209:etiology / Q000517:prevention & control*; D005765:Gastrointestinal Agents / Q000627:therapeutic use; D005997:Glycerylphosphorylcholine / Q000008:administration & dosage / Q000627:therapeutic use*; D007413:Intestinal Mucosa / Q000098:blood supply / Q000276:immunology / Q000378:metabolism; D007421:Intestine, Small / Q000098:blood supply* / Q000276:immunology / Q000378:metabolism; D008099:Liver / Q000098:blood supply / Q000276:immunology / Q000378:metabolism; D008297:Male; D065666:Mesenteric Ischemia / Q000503:physiopathology; D008833:Microcirculation; D018384:Oxidative Stress; D011897:Random Allocation; D017207:Rats, Sprague-Dawley; D026361:Reactive Nitrogen Species / Q000037:antagonists & inhibitors / Q000378:metabolism; D015427:Reperfusion Injury / Q000209:etiology / Q000276:immunology / Q000503:physiopathology / Q000517:prevention & control*; D013997:Time Factors
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D005765:Gastrointestinal Agents; D026361:Reactive Nitrogen Species; D005997:Glycerylphosphorylcholine; D000255:Adenosine Triphosphate