000120524 001__ 120524
000120524 005__ 20240228145450.0
000120524 0247_ $$2doi$$a10.1186/s12950-017-0150-y
000120524 0247_ $$2pmid$$apmid:28167864
000120524 0247_ $$2pmc$$apmc:PMC5288872
000120524 0247_ $$2altmetric$$aaltmetric:16060234
000120524 037__ $$aDKFZ-2017-00953
000120524 041__ $$aeng
000120524 082__ $$a610
000120524 1001_ $$aFraunberger, Peter$$b0
000120524 245__ $$aEzetimibe reduces cholesterol content and NF-kappaB activation in liver but not in intestinal tissue in guinea pigs.
000120524 260__ $$aLondon$$bBioMed Central$$c2017
000120524 3367_ $$2DRIVER$$aarticle
000120524 3367_ $$2DataCite$$aOutput Types/Journal article
000120524 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1524660044_18387
000120524 3367_ $$2BibTeX$$aARTICLE
000120524 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000120524 3367_ $$00$$2EndNote$$aJournal Article
000120524 520__ $$aStatins (HMG CoA reductase inhibitors), in addition to reducing circulating cholesterol and incidence of coronary heart disease, also have pleiotropic, anti-inflammatory effects. Patients with chronic liver diseases, non-alcoholic fatty liver disease (NAFLD) or hepatitis C are often excluded from statin therapy because of adverse effects in a small cohort of patients despite increased cardiovascular risk cholesterol. Ezetimibe, which inhibits cholesterol absorption by inhibition of Niemann-Pick C1 like 1 (NPC1L1) protein in the brush border of intestinal cells, has been suggested as a new therapeutic option in these patients.Effects of ezetimibe on lipoprotein metabolism, hepatic and intestinal lipid content in guinea pigs, an animal model with a lipoprotein profile and pattern similar to humans were investigated. In order to investigate a possible effect of ezetimibe on cholesterol induced inflammation NF-kappaB activation as an indicator for inflammatory processes in liver and gut tissue was measured.Lipid enriched diet led to accumulation of lipids in hepatic tissue which caused strong hepatic NF-kappaB activation. Ezetimibe reduced lipid diet induced increase of circulating cholesterol by about 77% and prevent hepatic NF-kappaB activation almost completely. In contrast in intestinal cells Ezetimibe, though lowering diet induced cholesterol accumulation, increased triglyceride content and subsequent NF-kappaB activation.In summary these data show, that ezetimibe effectively reduced diet induced circulating cholesterol levels, hepatic lipid accumulation and inflammatory response in our guinea pig model. However this drug elicited a local inflammatory response in intestinal tissue. Whether these diverse effects of ezetimibe on inflammatory parameters such as NF-kappaB have clinical relevance remains to be determined.
000120524 536__ $$0G:(DE-HGF)POF3-322$$a322 - Genetics and Pathophysiology (POF3-322)$$cPOF3-322$$fPOF III$$x0
000120524 588__ $$aDataset connected to CrossRef, PubMed,
000120524 7001_ $$0P:(DE-He78)b72c4ee15f75cf6944080c339a34475b$$aGröne, Elisabeth$$b1$$udkfz
000120524 7001_ $$0P:(DE-He78)00a2ea610aee4a8fca32908fc3d02e91$$aGröne, Hermann-Josef$$b2$$udkfz
000120524 7001_ $$aDrexel, Heinz$$b3
000120524 7001_ $$aWalli, Autar K$$b4
000120524 773__ $$0PERI:(DE-600)2164385-4$$a10.1186/s12950-017-0150-y$$gVol. 14, no. 1, p. 3$$n1$$p3$$tJournal of Inflammation$$v14$$x1476-9255$$y2017
000120524 909CO $$ooai:inrepo02.dkfz.de:120524$$pVDB
000120524 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)b72c4ee15f75cf6944080c339a34475b$$aDeutsches Krebsforschungszentrum$$b1$$kDKFZ
000120524 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)00a2ea610aee4a8fca32908fc3d02e91$$aDeutsches Krebsforschungszentrum$$b2$$kDKFZ
000120524 9131_ $$0G:(DE-HGF)POF3-322$$1G:(DE-HGF)POF3-320$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lHerz-Kreislauf-Stoffwechselerkrankungen$$vGenetics and Pathophysiology$$x0
000120524 9141_ $$y2017
000120524 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bJ INFLAMM-LOND : 2015
000120524 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000120524 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000120524 915__ $$0StatID:(DE-HGF)0501$$2StatID$$aDBCoverage$$bDOAJ Seal
000120524 915__ $$0StatID:(DE-HGF)0500$$2StatID$$aDBCoverage$$bDOAJ
000120524 915__ $$0LIC:(DE-HGF)CCBYNV$$2V:(DE-HGF)$$aCreative Commons Attribution CC BY (No Version)$$bDOAJ
000120524 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List
000120524 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000120524 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000120524 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews
000120524 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5
000120524 9201_ $$0I:(DE-He78)G130-20160331$$kG130$$lZelluläre und Molekulare Pathologie$$x0
000120524 980__ $$ajournal
000120524 980__ $$aVDB
000120524 980__ $$aI:(DE-He78)G130-20160331
000120524 980__ $$aUNRESTRICTED