Beta-Adrenergic Receptor 1 Selective Antagonism Inhibits Norepinephrine-Mediated TNF-Alpha Downregulation in Experimental Liver Cirrhosis 英文参考文献.docVIP

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Beta-Adrenergic Receptor 1 Selective Antagonism Inhibits Norepinephrine-Mediated TNF-Alpha Downregulation in Experimental Liver Cirrhosis 英文参考文献.doc

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Beta-Adrenergic Receptor 1 Selective Antagonism Inhibits Norepinephrine-Mediated TNF-Alpha Downregulation in Experimental Liver Cirrhosis 英文参考文献

Beta-AdrenergicReceptor1SelectiveAntagonism InhibitsNorepinephrine-MediatedTNF-Alpha DownregulationinExperimentalLiverCirrhosis PedroZapater1,2,IsabelGo′mez-Hurtado1,3,GloriaPeiro′4,Jose′ ManuelGonza′lez-Navajas1,3, IrmaGarc?′a1,3,PaulaGime′nez1,3,AlbaMoratalla1,3,Jose′ Such1,3,Rube′nFrance′s1,3 * 1The Biomedical Research Centre Network in the Area of Hepatic and Digestive Disorders (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain, 2Servicio de Farmacolog?′aCl?′nica,HospitalGeneralUniversitario,Alicante,Spain,3UnidadHepa′tica,HospitalGeneralUniversitario,Alicante,Spain,4UnidaddeInvestigacio′n,Hospital GeneralUniversitario,Alicante,Spain Abstract Background: Bacterial translocation is a frequent event in cirrhosis leading to an increased inflammatory response. Splanchnicadrenergicsystemhyperactivationhasbeenrelatedwithincreasedbacterialtranslocation.Weaimatevaluating the interacting mechanism between hepatic norepinephrine and inflammation during liver damage in the presence of bacterial-DNA. AnimalsandMethods:Forty-sixmicewereincludedina16-weekprotocolofCCl4-inducedcirrhosis.Laparotomieswere performed atweeks6, 10,13and16.Asecond setoffortymice injectedwithasingleintraperitonealdose ofCCl4 was treatedwithsaline,6-hydroxidopamine,NebivololorButoxamine.After5days,micereceivedE.coli-DNAintraperitoneally. Laparotomies were performed 24hours later. Liver bacterial-DNA, norepinephrine, TNF-alpha, IL-6 and beta-adrenergic receptorlevelsweremeasured. Results:Bacterial-DNAtranslocationwasmorefrequentinCCl4-treatedanimalscomparedwithcontrols,andincreasedas fibrosisprogressed.Livernorepinephrineandpro-inflammatorycytokinesweresignificantlyhigherinmicewithvswithout bacterial-DNA(319.76120.6vs120.7668.6pg/gfornorepinephrine,38.466.1vs29.764.2pg/gforTNF-alpha,41.867.4vs 28.764.3pg/gforIL-6).Onlybeta-adrenergicreceptor-1wassignificantlyincreasedintreatedvscontrolanimals(34.667.3 vs12.565.3,p=0.01)andcorrelatedwithTNF-alpha,IL-6andnorepinephrinehepaticleve