《Protein Kinase B Signal Pathway in Hepatic Fibrosis Rats.》.pdf

·438· ORIGINALARTICLE EffectsofGanfukang(肝复康)onExpressionofConnective TissueGrowthFactorandFocalAdhesionKinase／Protein KinaseBSignalPathwayinHepaticFibrosisRats ZHANGKun(张 坤) ，JIANGMiao．na(姜妙娜)，ZHANGCai-hua(张彩华)‘ LICong(李 骢)。，andJIAYu-jie(贾玉杰)。 ABsTRACT objective：ToinvestigatetheeffectofGanfukang(肝复康，GF}()onconnectivetissuegrowthfactor (CTGF)andfocaIadhesionkinase(FAK)／pr·oteinkinaseB (PKBorAkt)signalpathwayinahepaticfibrosisrat modeIandtoexploretheunderlyingtherapeuticmolecularmechanismsofGFK．Methods：FifIySDratswere randomlydividedintofivegroupsasfollows：thecontrolgroup，themodelgroup(repeatedsubcutaneousinjection ofCCI4)，andthethreeGFKtreatmentgroups(31．25，312．5，and3125mgk／g，intragastricadministration)．Reverse transcriptase．polymerasechainreaction(RT-PCR)，Westernblotting，andimmunohistochemistrywereusedto examinetheexpressionofcTGF，integrin0【5，integrin 131，FAK／Aktsignalpathway，cyclinD1，andcoilageninthe different-treatedrats．Results：GFKattenuatedtheup-regulationofCTGF，integrino1．5，andintegrin 131inhepatic fibrosisratsandsuppressedboththephosphorylationofFAKandthephosphorylationofAktsimultaneously (PO．01)．Atthesametime，theexpressionofcyclinD1，collagen I，andcollagenⅢwasdecreasedbyGFK significantly(PO．01)．Conclusions：CTGFandFA ktsignalpathwaywereactivatedintheCCI4-inducedhepatic fibrosisrats。whichcontributetoincreasedexpressionofcyclinD1andcollagengenes．Themechanismsofthe anti-fibrosisactivityofGFKmaybeduetoitseffectsagainstCTGFandFA ktsignaIpathway． KEYWORDS connectivetissuegrowthfactor，Ganfukang，hepaticfibrosis，FAKA／ktsignalpathway HepaticfibrosisisacommoncharacteristicOf someECM．producingcellse『．q．，fibroblastsandhepatic chronicIiverdiseases，representingamajorworldwide stellatecellsfHSCs)]．ItwasfoundthatCTGFcould medicalproblem．A wound-healingresponsetosome