Diethylnitrosamineinduced rat liver cancer model and pathological changes毕业论文翻译.docx

Diethylnitrosamineinduced rat liver cancer model and pathological changes毕业论文翻译.docx

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Diethylnitrosamineinducedratlivercancermodelandpathologicalchanges毕业论文翻译

Diethylnitrosamine-inducedratlivercancermodelandpathologicalchanges

Papertowritenetwork:

:

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.

[Keywords:

]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