Diethylnitrosamineinduced rat liver cancer model and pathological changes毕业论文翻译文档格式.docx
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Diethylnitrosamineinduced rat liver cancer model and pathological changes毕业论文翻译文档格式.docx
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LiXiaoYanwhitesaltyYongLiuShenHanYuzhenLiuLide
[Abstract]ObjectiveToestablishasimpleoccurrenceofasimilarprocessofdevelopmentoflivercanceranimalmodelsandhumanlivercancer.Methodsweighing150to200gmaleWistarratsof150wererandomlydividedintoexperimentalandcontrolgroups,theexperimentalgroupwasfedwithcontainingdiethylnitrosamine(DEN,80×
10-6),drinkingwater,changedtofreeaccesstowaterfor12weeks.controlgroupofconventionalfreeaccesstowater.theresultsofpathologicalexaminationconfirmedthatDEN-inducedlivercancerishepatocellularcarcinoma,inducedcancerrate70.6%(36/51,ratlivercancercarcinogenesisroughlythreestagesoflivercellinjuryofthelivercellproliferationsclerosisandmalignanttransformationofconclusionsfedlowdosesofDEN-inducedratlivercancermodeltobuildasuccessfulrate,isanidealstudyofhumanlivercancerinanimalmodels.
[Keywords:
]diethylnitrosamine,hepatocellularcarcinoma,rat,animalmodels[Abstract]ObjectiveToestablishanexperimentalhepatocellularcarcinomaratmodelwhichisconvenientandsimilartothehumanhepatocarcinogenesis.MethodsonehundredandfiftymaleWistarrats,weighing150to200g,wererandomlydividedintotwogroups.Theexperimentalgroup’sdrinkingwatercontained80ppmdiethylnitrosaminefor12continuousweeks.Thecontroldranktheroutinetablewater.Results70.6%(36/51)hepatocellularcarcinomawereinducedbyDEN.Theprocessionofhepatocarcinogenesisinthismodelincludedthreestageshepatictoxiclesion,hepaticproliferation/cirrhosisandhepaticcarcinogenesis.ConclusionThesuccessfulrateoflivercancermodelinducedbylowdoseDENwashigh,itisanidealexperimentalmodelforthestudyofhepatocarcinogenesis.
]Diethylnitrosamine,hepatocellularcarcinoma,rat,animalmodelHepatocellularcarcinoma(ofhepatocellularcarcinoma,HCCisoneofthecommonmalignanttumors,knownas“cancer”fromtheperspectiveoftumorimmunology,molecularbiologyandmolecularpathologytostudytheoccurrence,thelawofdevelopment,andmolecularmechanism,oftensubjecttotheconstraintsofclinicalspecimens.inlivercancerbasicresearch,weneedtochooseasuitablelivercanceranimalmodeltosimulatetheprocessofhumanliverdiseasetocompensateforthelackofclinicalspecimens.Thisarticledescribescomparedwithlongperiodofapplicationoflowdosesofdiethylnitrosamine-inducedpathologicalchangesinrathepatomamodelandtheprocessofcarcinogenesis.
1Materialsandmethods1.1Drugdiethylnitrosamine,0.95g/ml99.9%purity,Sigma,USA.MaleWistarratsofcleangradeof1.2inexperimentalanimals150AnimalCertificateofConformity:
SCXK(Lu)20030004],weighing150to200g,werepurchasedfromtheExperimentalAnimalCenterofShandongUniversity.Allratsweredividedcagerearing,useofstandardizedlight,freedomeating,regularreplacementofthelitter,andadapttotheenvironmentfor7days.alltheratsweredividedintoarandomnumbertable,theexperimentalgroup(135)andthecontrolgroup(15.
FeedcontainingbyDEN(80×
10-6drinkingwaterfor1.3experimentalmethodexperimentalgroup,12weeksintofreedrinkingwater.Controlgroup,conventionalfreeaccesstowaterdailyobservationoftheanimal’smentalstate,dietandbackgrosschangesingeneral.experimentalsection4,8,12,16,18,20,22,24,25weekswererandomlyselectedfromthemodelgroup10to15,theabdominalcavitywasopened,thegeneralobservationoftheexposedliver,therecordofthelivershape,color,texture.liverspecimens,4%paraformaldehydebuffer,fixedfor24h,embeddedinparaffinsections,HEstaining,observedunderthemicroscope.controlgroupweretakenat4,12and24weeks5tobetreatedinthesame.
2Results2.1GeneralsituationofcarcinogenesisfourweeksaftertheexperimentalgroupofWistarratsfoodintakedecreased,andthegradualemergenceofthecoatdullyellow,dull,slow,slowgrowthofbodyweightthanthecontrolgroup,somebodyweightofratsissignificantlylowerself-inducedcancer,thefirstsevenweeks,experimentalratsbegantodeath,totaldeathof24Wistarrats,inparticularparagraphs17,18weeksand21to25weeksmoredeadrats,themortalityratewas17.78%(24/135.controltheratsgrewwell,nosignificantpathologicalperformance.
2.2inducedcarcinogenesisinratliverpathologicalchanges2.2.1controlgroupratswerenoobviousabnormalities:
livernakedeyeviewofthelightmicroscope,livertissuewasnormal,thelivercellsarrangedincordsaroundthecentrallobularveinradiallyarrangedhepatocyteseosinophiliccytoplasm,nuclearbasophilic,mostlyforsingle-core,locatedinthecellcenter(seeFigure1.
2.2.2experimentalrats:
experimentalratsliverpathologicalchangescanbebroadlygroupedintothree:
①inducedcancerearly-livercellinjuryperiod:
1to8weeks(n=30.Livershowednoabnormaltableviewthelightmicroscope,swellingofthelivercells,showingdiffuselivercelledema,thepartofthelivercellswaseosinophilicchronotropic(seeFigure2.lobulestructureisstillintactandvisiblefocallobularnecrosiswithinflammatorycellinfiltration,whilegraduallyfibroustissueproliferationandregeneration.②carcinogenesisinterim-sclerosisperiod:
9to16weeks(n=30liversurfacegraduallyrough,therevaryingamounts,largeandsmallgraynear-circularlesiondiametermostlybelow1mm,maximumuptoabout5mm,moredispersed(seeFigure3.first16weeksofcirrhosis,partofthelobeofcholestasis.lightmicroscope,furtheraggravatingthelivercelledema,visiblevesiclesofdifferentdegreesofsteatosis.
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eosinophilicorclearcellfoci(Figure4),andgraduallyformedthenodulesoflivercellproliferation,cellularatypiasmallernodulesonthesurroundingorganizationsoppression(seeFigure5.twocasesshowedanoduleofatypicalhyperplasia,nodularlivercelldysplasiaobviouscellnodulesoccasionallymitoticandnucleolarproliferation(seeFigure6.portalveindilatationandcongestion,therearevaryingdegreesofovalcellproliferationandhyperplasiaofconnectivetissueextendedtothelobules,alongwithbileducthyperplasia,increasednumberofvisiblethetypicalpseudolobuleform(seeFigure7.③latecarcinogenesis-cancerof12weeksonecasesofratperitonealvivisection:
17to25weeks(n=51graynodulesoftheliversurfacecoveredwithseveraldifferentsizes,andthelargest4.5cm×
3cm×
2cm,thesectioncanbeseenbleedingandnecrosis.appearwithinthehemorrhagicascites,deadratsintheprocessofcarcinogenesis.1casesofbloodyascitesgreateromentumintwocasesofintra-abdominaldiffusenodularliverwithadhesion.lightmicroscope,livercancercellswerearrangedinbeamcordsandmassiveinfiltrationtothesurroundinglivertissue,canbeseenvaryingdegreesoffattydegeneration,someareasofhemorrhage,necrosis(seeFigure8.cancertissueedema,eosinophilicchange,fattydegeneration,andfocioflivercellproliferationResultssectionandatypicalhyperplasianodularhistologicalmaintypesofhepatocellularcarcinoma,andonecasesofmixedcellcarcinoma
2.3carcinogenesisprocessinvariousstagesoflesiontypeandlesiontypeandincidenceofthevariousstagesoftheincidenceofDEN-inducedratlivercancerinTable1.
3
Livercanceranimalmodelofchoiceisanimportantpartoflivercancerexperimentalstudiessincetheearly1900s,thedeepeningofspontaneoushepatocellularcarcinomainmicemodelsoflivercanceranimalmodel,therehasbeenresearch,andgraduallyestablishedaspontaneousanimallivercancermodelinducedlivercancermodel,thetransplantedanimallivercancermodel,aswellastransgenicanimallivercancermodel.avarietyoflivercanceranimalmodelhasitsowncharacteristicsanduses,theappropriatechoiceoflivercanceranimalmodelaccordingtothestudypurpose.
Inducedlivercancermodelisacarcinogenicchemical,physical,orbiologicalfactorsoftheformationoflivercancerinanimalmodels.Amongthem,theDEN-inducedanimallivercancerisabroaderapplicationofaninducedlivercancermodel.ByDENforinternationalCancerResearchCenterinstitutions(Internationalagencyforresearchoncancer,carcinogensidentifiedbyIARC,thedualroleofinitiationandpromotionoftumorigenesis.applicationofDEN-inducedratlivercancermodelgenerallygavageonceaweek0.25%byDENaqueoussolution10mg/kgbodyweight,theremaining6dfeddrinkingwaterto0.025%byDEN[1],ortransoralintubationwerefed0.2%byDENsolution,1mlofaday,aweekcontinuouslyfedfor4d,continuousfed18weeksafterdiscontinuation[2],or5timesaweek,ratsweregiven0.2%byDEN(10mg/kg,administeredorally,modelingtheway[3],butsuchmethodismoredifficult,andlong-termfeedingonlargeThemousebodyhasacertaindegreeofdamage,easilyleadtothemouthanddigestivetractinfections.
Inthisstudy,thefeedcontainingbyDEN(80×
10-6water-inducedratlivercancermodel,hasthefollowingcharacteristics:
①operationmoreconvenient,shortercycletimes,inducedcancerrate(72.5%
(2)carcinogenicthantheloyal,hepatocellularcarcinomaproportionaccountedfor97.3%(37casesofinducedcancer,onlyonecaseofmixed-cellcarcinoma,alltherestofHCC.③cancerousprocess,theprocessofcirrhosis,themid-carcinogenesiscirrhosiswas23.3%,17.6%incarcinogenesisofhepatocellularcarcinomawithcirrhosis,thepathologica
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