• Marianne Landmann, Giridhar Kanuri, Astrid Spruss, Carolin Stahl, and Ina Bergheim.
• SD Model Systems of Molecular Nutrition, Friedrich-Schiller University, Jena, Germany.
• Nutrition. 2014 Jul 1; 30 (7-8): 882889882-9.

ObjectiveAcute and chronic consumption of alcohol can alter intestinal barrier function thereby increasing portal endotoxin levels subsequently leading to an activation of toll-like receptor (TLR) 4-dependent signaling cascades, elevated levels of reactive oxygen species and induction of tumor necrosis factor α in the liver. Recent studies suggest that chicoric acid found in Echinacea pupurea, chicory, and other plants, may possess antioxidant and anti-inflammatory effects. The aim of the present study was to determine if chicoric acid can reduce acute alcohol-induced liver damage.MethodsFemale mice were given chicoric acid orally (4 mg/kg body weight) for 4 d before acute ethanol administration (6 g/kg body weight). Furthermore, the effect of chicoric acid on the lipopolysaccharide (LPS)-dependent activation in an in vitro model of Kupffer cells (RAW264.7 macrophages) was assessed.ResultsAcute alcohol ingestion caused a significant increase in hepatic triacylglycerols accumulation, which was associated with increased protein levels of the inducible nitric oxide synthase (iNOS), 4-hydroxynonenal protein adducts, and active plasminogen activator inhibitor 1 protein in the liver. Pretreatment of animals with chicoric acid significantly attenuated these effects of alcohol on the liver. In LPS-treated RAW264.7 macrophages, pretreatment with chicoric acid significantly suppressed LPS-induced mRNA expression of iNOS and tumor necrosis factor α.ConclusionThese data suggest that chicoric acid may reduce acute alcohol-induced steatosis in mice through interfering with the induction of iNOS and iNOS-dependent signaling cascades in the liver.Copyright © 2014 Elsevier Inc. All rights reserved.

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