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1、Experimentalstudyontheeffectofanti-hepaticfibrosisofDiisopropylamineDichloroacetateAbstractExperimentalstudyontheeffectofanti-hepaticfibrosisofDiisopropylamineDichloroacetateAbstractObjective:1.Tostudytheeffectofdiisopropylaminedichloroacetate(DPDA)ontheproliferationofLX2andLO2cellsinvitro.2.Toinves
2、tigatethefibrosisreverseeffectofDPDAtoCCl4-inducedhepaticfibrosismiceinvivo.Method:1.Invitro,MTTassaywasusedtodeterminethegrowthinhibitionofLX2andLO2cells,andWesternBlotwasperformedtoinvestigatetheindicatorsrelatedtohepaticfibrosis.2.Invivo,fiftymaleC57BL/6micewererandomlyallocatedtothreegroups,thec
3、ontrolgroup(n=10),theCCl4group(n=30)andtheDPDA+CCl4group(n=10).ThemodelofliverfibrosiswasinducedbyintraperitondalinjectionwithCCl4(2ul/gbodyweightdissolved1:3incornoil)twotimesperweeklastingfor12weeksinCCl4groupandtheDPDA+CCl4group.After8weeksinjectionwithCCl4,miceweretakenDPDAbyintragastricadminist
4、rationinDPDA+CCl4group.Meanwhile,miceinCCl4groupwereonlytakenPBSbyintragastricadministration.ThedegreeofliverfibrosiswasassessdebyHEandMasson’sstaining.Meanwhile,PCR、Immunohistochemistry、WesternBlotwereusedtodetectmRNAandproteinlevelsofalpha-soothmuscleactin(α-SMA)、desmin、Ki67、transforminggrowthfact
5、or-beta1(TGF-β1)、fibronectin(FN)、typeIcollagen.Results:AfterDPDAwasaddedtoLX2andLO2for48h,DPDAcouldinhibititsproliferation,IC50was（13.2±0.71）mmol/l;however,DPDAcouldfacilitatetheproliferationofLO2whentheconcentrationwasbelow1mmol/l;differencebetweenthegroupswasstatisticallysignificant(P<0.05).HEandM
6、assonstainshowedthatliverdamagewasalleviatedinDPDA+CCl4group.Meanwhile,PCR、Immunohistochemistry、WesternBlotshowedthattheexpressionsofalpha-soothmuscleactin(α-SMA)、desmin、Ki67、transforminggrowthfactor-beta1(TGF-β1)、fibronectin(FN)andtypeIcollagenIIIAbstractExperimentalstudyontheeffectofanti-hepaticfi
7、brosisofDiisopropylamineDichloroacetateweredownregulatedInDPDA+CCl4group.Conclusion:1.DPDAcouldinhibittheproliferationofLX2cells,butfacilitatetheproliferationofLO2cells.2.DPDAwascapableofinhibitingCCl
