生姜提取物6-姜酚對乙酰氨基酚致小鼠肝臟毒性的保護(hù)作用

生姜提取物6-姜酚對乙酰氨基酚致小鼠肝臟毒性的保護(hù)作用

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mentalmiceweredecapitated4haftertheacetaminopheninjection;thetrunkbloodwascollectedandtheserumwasseparatedandstoredat-70℃.Tissuesamplesfromtheliverswereobtainedforbiochemicalanalysis.1.5utilizesinrectity相關(guān)概念Theactivitiesofalkalinephosphatase(ALP),alanineandaspartateaminotransferases(ALTandAST)andtotalbilirubininserumwereestimatedbyusingcommericialkits(SpanDiagnostics,Chennai,India).Inthehepatictissuesamples,lipidperoxidationwasmeasuredusingthiobarbituricacidreactivesubstances(TBARS)accordingtothemethodofOhkawaetal.Thelipidperoxidationwasexpressedasmicromolesofthiobarbituricacid(TBA)reactantsper100goftissuehomogenate.Superoxidedismutase(SOD)wasestimatedinliverhomogenateaccordingtothemethodofMarklundetal.Catalase(CAT)wasassayedbythemethodofSinha.Glutathioneperoxidase(GPx)wasassayedbythemethodofRotrucketal.Glutathionereductase(GR)thatutilizesnicotinamideadeninedinucleotidephosphate(NADPH)toconvertoxidizedglutathione(GSSG)tothereducedformwasassayedbythemethodofBellomoetal.Glutathionetransferase(GST)wasassayedbythemethodofHabigetal.Totalreducedglutathione(GSH)wasdeterminedbythemethodofMoronetal.TheproteincontcntwasdeterminedbythemethodofLowryetalusingbovineserumalbuminasastandard.1.6StatisticalanalysisResultswereexpressedasmean±standarddeviationandthestatisticalanalysiswasperformedusinganalysisofvariance,todeterminethesignificantdifferencesbetweenthegroups,followedbyStudent-Newman-Keulstest.P<0.05impliedsignificance.2產(chǎn)品系統(tǒng)2.1國際習(xí)慣法國際習(xí)慣法ThelevelsofTBARSformation,SOD,CAT,GPx,GR,GSTandtotalreducedGSHinliverofcontrolandexperimentalmicewereshowninTable1.Inacetaminophcn-trcatedmice,SOD,CAT,GPx,GR,GSTandtotalreducedGSHwerefoundtobedecreased,whereasTBARSlevelwereincreasedcomparedwiththecontrolgroup(P<0.05).However,treatmentof6-gingeroltoacetaminophen-inducedmicealteredtheabovechangesbyregulatingtheTBARSlevelandantioxidantenzymes(P<0.05).2.2國際醫(yī)學(xué)單一標(biāo)準(zhǔn)下國際ast新型細(xì)胞術(shù)TheactivitiesofALT,ASTandALPandcontentoftotalbilirubininserumofcontrolandexperimentalgroupswereshowninTable2.TheactivitiesofALT,ASTandALPandcontentoftotalbilirubininserumweresignificantlyincreasedinacetaminophen-inducedmicecomparedwithcontrolgroup(P<0.05).However,6-gingeroltreatmentpreventedtheabovechangesobservedinacetaminophen-inducedmice(P<0.05).3indexhatching.治療前后Inthisstudy,weinvestigatedtheeffectof6-gingerolagainstacetaminophen-inducedliverdamageinmice.Noticeableindicationofliverinjuryisthereleaseofcellularenzymesintotheplasmaduetotheinterruptioncausedbychemicalsinthetransportfunctionsofthehepatocytes.Theevaluationofenzymesintheserumismarkerforliverdamage.Inthepresentstudy,acetaminophenadministrationcausedasignificantincreaseinlivermarkerenzymesAST,ALTandALP,totalbilirubinandlipidperoxidationcomparedwiththenormalmice.Theturnaroundofincreasedserumenzymes,totalbilirubinandlipidperoxidationobservedin6-gingeroI-treatedacetaminophenintoxicatedmicewassupportedbythelimiteddegreeofhistologicalchanges.Thereversaloftransaminaseslevelinserumwiththehealingofhepaticparenchymaandtheregenerationofhepatocytesiscommonlyacceptedagreement.Thishepatoprotectiveeffectof6-gingerolmaybeduetothepreventionoftheintracellularenzymereleasebyitsmembranestabilizingandantioxidantactivity.LargedoseofacetaminophencauseshepaticglutathionedepletionbecauseexcessNAPQIreactsrapidlywithGSHwhichexacerbatesoxidativestressinconjunctionwithmitochondrialdysfunction.TheNAPQI-induceddepletionofcytosolicandmitochondrialGSHtriggerthelossofcellularhomeostasisleadingtoliverinjury.TheactionsofSOD,CAT,andGPxareinsightfulindexesinhepatorenaldamageastheyscavengethereactiveoxygenspeciesleadingtodiminishingofthetoxiceffects.Inconsistencewithourpreviousreport,inthispresentstudy,acetaminopheninduction(900mg/kgbodyweight)significantlyincreasedthelipidperoxidationlevels,andcausedthedepletionofantioxidantstatus(SOD,CAT,GPx,GR,GSTandGSH).However,treatmentwith6-gingerolandsilymarinabrogatedtheacetaminopheninduceddecreasesinantioxidantenzymesandGSHinmice.TherestoredhepaticGSHlevelobservedinacetaminophen-inducedmiceindicatesaninvolvementof6-gingerolinfacilitatingtherapidandefficientconsumptionofreactiveoxygenspeciesgeneratedbyacetaminophenP450bioactivation.Therefore,theobservedantioxidantprotectionfrom6-gingerolagainstacetaminophen-inducedhepatotoxicitymightbepartiallyduetotheincreasedGSH.Arecentstudyhasshownthatgingerisgiftedwithstrongantioxidanteffectsagainstacetaminophen-inducedhepatotoxicity.Theantioxidantactionobservedbythe6-gingerolinourstudyisinaccordancewitht