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Status: Bibliographieeintrag

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Verfasst von:Patsenker, Eleonora [VerfasserIn]   i
 Stoll, Matthias [VerfasserIn]   i
 Millonig, Gunda [VerfasserIn]   i
 Agaimy, Abbas [VerfasserIn]   i
 Wissniowski, Till [VerfasserIn]   i
 Schneider, Vreni [VerfasserIn]   i
 Mueller, Sebastian [VerfasserIn]   i
 Brenneisen, Rudolf [VerfasserIn]   i
 Seitz, Helmut K. [VerfasserIn]   i
 Ocker, Matthias [VerfasserIn]   i
 Stickel, Felix [VerfasserIn]   i
Titel:Cannabinoid receptor type I modulates alcohol-induced liver fibrosis
Verf.angabe:Eleonora Patsenker, Matthias Stoll, Gunda Millonig, Abbas Agaimy, Till Wissniowski, Vreni Schneider, Sebastian Mueller, Rudolf Brenneisen, Helmut K. Seitz, Matthias Ocker, and Felix Stickel
E-Jahr:2011
Jahr:19 August 2011
Umfang:10 S.
Fussnoten:Gesehen am 23.09.2022
Titel Quelle:Enthalten in: Molecular medicine
Ort Quelle:[London] : BioMed Central, 1994
Jahr Quelle:2011
Band/Heft Quelle:17(2011), 11/12, Seite 1285-1294
ISSN Quelle:1528-3658
Abstract:The cannabinoid system (CS) is implicated in the regulation of hepatic fibrosis, steatosis and inflammation, with cannabinoid receptors 1 and 2 (CB1 and CB2) being involved in regulation of pro- and antifibrogenic effects. Daily cannabis smoking is an independent risk factor for the progression of fibrosis in chronic hepatitis C and a mediator of experimental alcoholic steatosis. However, the role and function of CS in alcoholic liver fibrosis (ALF) is unknown so far. Thus, human liver samples from patients with alcoholic liver disease (ALD) were collected for analysis of CB1 expression. In vitro, hepatic stellate cells (HSC) underwent treatment with acetaldehyde, Δ9-tetrahydrocannabinol H₂O₂, endo- and exocannabinoids (2-arachidonoylglycerol (2-AG) and [THC]), and CB1 antagonist SR141716 (rimonabant). In vivo, CB1 knockout (KO) mice received thioacetamide (TAA)/ethanol (EtOH) to induce fibrosis. As a result, in human ALD, CB1 expression was restricted to areas with advanced fibrosis only. In vitro, acetaldehyde, H₂O₂, as well as 2-AG and THC, alone or in combination with acetaldehyde, induced CB1 mRNA expression, whereas CB1 blockage with SR141716 dose-dependently inhibited HSC proliferation and downregulated mRNA expression of fibrosis-mediated genes PCα1(I), TIMP-1 and MMP-13. This was paralleled by marked cytotoxicity of SR141716 at high doses (5-10 μmol/L). In vivo, CB1 knockout mice showed marked resistance to alcoholic liver fibrosis. In conclusion, CB1 expression is upregulated in human ALF, which is at least in part triggered by acetaldehyde (AA) and oxidative stress. Inhibition of CB1 by SR141716, or via genetic knock-out protects against alcoholic-induced fibrosis in vitro and in vivo.
DOI:doi:10.2119/molmed.2011.00149
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.2119/molmed.2011.00149
 DOI: https://doi.org/10.2119/molmed.2011.00149
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Acetaldehyde
 Animals
 Apoptosis
 Cannabinoids
 Cell Hypoxia
 Cell Proliferation
 Collagen
 Female
 Hepatic Stellate Cells
 Humans
 Hydrogen Peroxide
 Inflammation
 Liver
 Liver Cirrhosis, Alcoholic
 Male
 Matrix Metalloproteinases
 Mice
 Middle Aged
 Piperidines
 Pyrazoles
 Receptor, Cannabinoid, CB1
 Receptor, Cannabinoid, CB2
 Rimonabant
 RNA, Messenger
 Up-Regulation
K10plus-PPN:181735194X
Verknüpfungen:→ Zeitschrift

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