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Effects of green tea catechins on the pro-inflammatory response after haemorrhage/resuscitation in rats

Relja, Borna ; Töttel, Eva ; Breig, Lara ; Henrich, Dirk ; Schneider, Heinz ; Marzi, Ingo ; Lehnert, Mark

In: British Journal of Nutrition, 2011, vol. 105, no. 12, p. 1791-1797

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    Titre
    • Effects of green tea catechins on the pro-inflammatory response after haemorrhage/resuscitation in rats
    Auteur
    • Relja, Borna. Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, 60590 Frankfurt, Germany
    • Töttel, Eva. Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, 60590 Frankfurt, Germany
    • Breig, Lara. Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, 60590 Frankfurt, Germany
    • Henrich, Dirk. Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, 60590 Frankfurt, Germany
    • Schneider, Heinz. HealthEcon AG, Steinentorstrasse 19, CH-4051 Basle, Switzerland
    • Marzi, Ingo. Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, 60590 Frankfurt, Germany
    • Lehnert, Mark. Department of Trauma, Hand and Reconstructive Surgery, Hospitals of the Johann Wolfgang Goethe-University, Frankfurt am Main, 60590 Frankfurt, Germany
    Type de document
    • Postprint
    Langue
    • Inglese
    Publié dans
    • British Journal of Nutrition, 2011, vol. 105, no. 12, p. 1791-1797. Cambridge University Press
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:294412
    Summary
    Plant polyphenols, i.e. green tea extract (GTE), possess high antioxidative and anti-inflammatory capacity, thus being protective in various models of acute inflammation. However, their anti-inflammatory effect and a feasible mechanism in haemorrhage/resuscitation (H/R)-induced liver injury remain unknown. We investigated the effects of GTE and the role of NF-κB in the pathogenesis of liver injury induced by H/R, and their effects on intercellular adhesion molecule-1 (ICAM-1) expression and neutrophil infiltration. Female Lewis rats were fed a standard chow diet (control, ctrl) or a diet containing 0·1% polyphenolic GTE for five consecutive days before H/R. Rats were haemorrhaged to a mean arterial pressure of 30 (sem 2)mmHg for 60min and resuscitated. Control groups (sham_ctrl and sham_GTE) underwent surgical procedures without H/R. At 2h after resuscitation, tissues were harvested. Serum alanine aminotransferase (ALT) and IL-6 were measured. Hepatic necrosis, ICAM-1 expression and polymorphonuclear leucocyte (PMNL) infiltration were assessed. Hepatic expression of IκBα (phospho) was measured. H/R induced strong liver damage with increased necrosis and serum ALT levels. Compared with both sham groups, inflammatory markers (serum IL-6 and hepatic PMNL infiltration) were elevated after H/R (P<0·05). Also, H/R increased IκBα phosphorylation. GTE administration markedly (P<0·05) decreased serum ALT and IL-6 levels, hepatic necrosis as well as PMNL infiltration and the expression of ICAM-1 and phosphorylated IκBα compared with H/R. In conclusion, we observed that NF-κB activation plays an important role in the pathogenesis of liver injury after H/R through the up-regulation of hepatic ICAM-1 expression and subsequent PMNL infiltration. GTE pre-treatment prevents liver damage in this model of acute inflammation through a NF-κB-dependent mechanism