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Gut-brain chemokine changes in portal hypertensive rats |
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| Authors: | Merino Joaquin Aller Maria-Angeles Rubio Sandra Arias Natalia Nava Maria-Paz Loscertales Maria Arias Jaime Arias Jorge-Luis |
| Affiliation: | 1. Department of Surgery I, School of Medicine, Complutense University of Madrid, Plaza de Ram??n y Cajal s.n, 28040, Madrid, Spain 3. Department of Psychobiology, School of Psychology, Autonomous University of Madrid, 28049, Cantoblanco, Madrid, Spain 4. Neurosciences Laboratory, School of Psychology, University of Oviedo, Pza. de Feijoo s/n, 33003, Oviedo, Asturias, Spain 5. Department of Physiology (Animal Physiology II), School of Biology, Complutense University of Madrid, J. A. Novais 2, 28040, Madrid, Spain 6. Department of Surgery, Massachusetts General Hospital, 1055 Fruit St., Boston, MA, 02114, USA |
| Abstract: | BackgroundHepatic encephalopathy is a syndrome whose physiopathology is poorly understood; therefore, current diagnostic tests are imperfect and modern therapy is nonspecific. Particularly, it has been suggested that inflammation plays an important role in the pathogenesis of portal hypertensive encephalopathy in the rat.AimWe have studied an experimental model of portal hypertension based on a triple partial portal vein ligation in the rat to verify this hypothesis.MethodsOne month after portal hypertension we assayed in the splanchnic area (liver, small bowel and mesenteric lymph nodes) and in the central nervous system (hippocampus and cerebellum) fractalkine (CX3CL1) and stromal cell-derived factor alpha (SDF1-??) as well as their respective receptors (CX3CR1 and CXCR4) because of their key role in inflammatory processes.ResultsThe significant increase of fractalkine in mesenteric lymph nodes (P?P?P?P?P?Conclusion The present study revealed that portal hypertension is associated with splanchnic-brain inflammatory alterations mediated by chemokines. |
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