title: A lipid anchor improves the protective effect of ectoine in inflammation.
abstract: Others and we have shown in several studies that the natural tetrahydropyrimidine ectoine protects mammalian cells and tissues against various stress factors including ischemia/reperfusion injury, UV-irradiation, and inflammation. Since little is known about the molecular mechanism of this protective effect, which was ascribed exclusively to an extracellular action of this small water-soluble molecule, we asked whether and how a hydrophobic anchor modulates the inflammation protective properties of ectoine. We therefore investigated the influence of ectoine and of its semi-synthetic derivative lauryl-ectoine on inflammation in RAW 264.7 macrophages and primary cultured rat intestinal smooth muscle (RISM) cells. Both, ectoine and lauryl-ectoine considerably decreased lipopolysaccharide (LPS)-induced interleukin (IL)- 1, IL-6, tumor necrosis factor (TNF)- α, and cyclooxygenase (COX)-2 gene expression in macrophages as well as TNF-α- induced IL-1, IL-6 and COX-2 expression in RISM cells. This reduction of inflammatory agents was accompanied on the one hand by a significant decrease of nuclear translocation of nuclear factor (NF)-κB and on the other hand by a reduction of cellular ceramide content. Interestingly, lauryl- ectoine was much more active exerting its effect at about 10-fold lower concentrations than its natural counterpart. Note that ectoine was almost completely recovered in the medium whereas lauryl-ectoine was found to be cell-associated. Together our data indicate that a lipid anchor considerably improves a possible preventive and/or therapeutic implementation of ectoine in inflammatory processes.
authors.forename: A
authors.initials: A
authors.lastname: Wedeking
authors.forename: N
authors.initials: N
authors.lastname: Hagen-Euteneuer
authors.forename: M
authors.initials: M
authors.lastname: Gurgui
authors.forename: R
authors.initials: R
authors.lastname: Broere
authors.forename: G
authors.initials: G
authors.lastname: Lentzen
authors.forename: R H
authors.initials: RH
authors.lastname: Tolba
authors.forename: E
authors.initials: E
authors.lastname: Galinski
authors.affiliation: University of Bonn, Gerhild van Echten-Deckert, Bonn, Germany. g.echten.deckert@uni-bonn.de.
authors.forename: G
authors.initials: G
authors.lastname: van Echten-Deckert
mesh_terms: D000599:Amino Acids, Diamino / Q000737:chemistry / Q000494:pharmacology*; D000818:Animals; D002460:Cell Line; D051546:Cyclooxygenase 2 / Q000276:immunology; D015870:Gene Expression; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism; D007375:Interleukin-1 / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D050356:Lipid Metabolism / Q000187:drug effects; D008264:Macrophages / Q000276:immunology; D051379:Mice; D016328:NF-kappa B / Q000276:immunology; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D000599:Amino Acids, Diamino; D007375:Interleukin-1; D015850:Interleukin-6; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; C045628:ectoine; D051546:Cyclooxygenase 2