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URN: urn:nbn:de:kobv:517-opus-16716
URL: http://opus.kobv.de/ubp/volltexte/2008/1671/
Püschel, Gerhard P. ;
Hespeling, Ursula ;
Oppermann, Martin ;
Dieter, Peter
Increase in prostanoid formation in rat liver macrophages (Kupffer cells) by human anaphylatoxin C3a
Kurzfassung in Englisch
Human anaphylatoxin C3a increases glycogenolysis in perfused rat liver. This action is inhibited by prostanoid synthesis inhibitors and prostanoid antagonists. Because prostanoids but not anaphylatoxin C3a can increase glycogenolysis in hepatocytes, it has been proposed that prostanoid formation in nonparenchymal cells represents an important step in the C3a-dependent increase in hepatic glycogenolysis. This study shows that (a) human anaphylatoxin C3a (0.1 to 10 mug/ml) dose-dependently increased prostaglandin D2, thromboxane B, and prostaglandin F2alpha formation in rat liver macrophages (Kupffer cells); (b) the C3a-mediated increase in prostanoid formation was maximal after 2 min and showed tachyphylaxis; and (c) the C3a-elicited prostanoid formation could be inhibited specifically by preincubation of C3a with carboxypeptidase B to remove the essential C-terminal arginine or by preincubation of C3a with Fab fragments of a neutralizing monoclonal antibody. These data support the hypothesis that the C3a-dependent activation of hepatic glycogenolysis is mediated by way of a C3a-induced prostanoid production in Kupffer cells.
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Freie Schlagwörter (Englisch): |
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lactate output , glucose , complement , flow , prostaglandin-f2-alpha |
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Institut 1: |
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Institut für Ernährungswissenschaft |
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Institut 2: |
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Extern |
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DDC-Sachgruppe: |
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Biowissenschaften, Biologie |
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Dokumentart: |
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c Postprint |
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Schriftenreihe: |
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Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe, ISSN 1866-8372 |
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Bandnummer: |
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paper 037 |
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Quelle: |
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Hepatoloy. - ISSN 0270-9139. - 18 (1993), 6, p. 1516 - 1521 |
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Sprache: |
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Englisch |
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Erstellungsjahr: |
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1993 |
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Publikationsdatum: |
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10.03.2008 |
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Bemerkung: |
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first published in: Hepatology - 18 (1993), 6 p. 1516 - 1521
ISSN: 0270-9139 doi: 10.1002/hep.1840180634
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Lizenz: |
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Keine Nutzungslizenz vergeben - es gilt das deutsche Urheberrecht
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