简介：AIM:Toevaluatethecorrelationofshearwaveelastography(SWE)resultswithliverfibrosishistologyandquantitativefunctionreserve.METHODS:Weeklysubcutaneousinjectionof60%carbontetrachloride(1.5mL/kg)wasgivento12caninesfor24wktoinduceexperimentalliverfibrosis,witholiveoilgivento2controlcanines.At24wk,liverconditionwasevaluatedusingclinicalbiochemistryassays,SWEimaging,lidocainemetabolitemonoethylglycine-xylidide(MEGX)test,andhistologicfibrosisgrading.Clinicalbiochemistryassayswereperformedattheinstitutionalcentrallaboratoryforroutineliverfunctionevaluation.Liverstiffnesswasmeasuredintriplicatefromthreedifferentintercostalspacesandexpressedasmeanliverstiffnessmodulus(LSM).PlasmaconcentrationsoflidocaineanditsmetaboliteMEGXweredeterminedusinghigh-performanceliquidchromatographyrepeatedinduplicate.Liverbiopsysampleswerefixedin10%formaldehyde,andliverfibrosiswasgradedusingthemodifiedhistologicalactivityindexKnodellscore(F0-F4).Correlationsamonghistologicgrading,LSM,andMEGXmeasureswereanalyzedwiththePearsonlinearcorrelationcoefficient.RESULTS:At24wkliverfibrosishistologicgradingwasasfollows:F0,n=2(control);F1,n=0;F2,n=3;F3,n=7;andF4,n=2.SWELSMwaspositivelycorrelatedwithhistologicgrading(r=0.835,P<0.001).Specifically,theF4grouphadasignificantlyhigherelasticmodulusthantheF3,F2,andF0groups(P=0.002,P=0.003,andP=0.006,respectively),andtheF3groupalsohadasignificantlyhighermodulusthanthecontrolF0group(P=0.039).LSMwasnegativelyassociatedwithplasmaMEGXconcentrationsat30min(r=-0.642;P=0.013)and60min(r=-0.651;P=0.012),timeto?ofthemaximumconcentration(r=-0.538;P=0.047),andtheareaunderthecurve(r=-0.636;P=0.014).Multiplecomparisonsshowedidenticaldifferencesinthesethreemeasures:significantlylowerwithF4(P=0.037)andF3(P=0.032)ascomparedtoF0a

简介：AIM:Todeterminethealterationsinratenterocytemitochondrialrespiratoryfunctionandenzymeactivitiesfollowingtraumaticbraininjury(TBI).METHODS:Fifty-sixmaleSDratswererandomlydividedintosevengroups(8ratsineachgroup):acontrolgroup(ratswithshamoperation)andtraumaticbraininjurygroupsat6,12,24h,days2,3,and7afteroperation.TBImodelswereinducedbyFeendy’sfree-fallingmethod.Mitochondrialrespiratoryfunction(respiratorycontrolratioandADP/Oratio)wasmeasuredwithaClarkoxygenelectrode.TheactivitiesofrespiratorychaincomplexⅠ-Ⅳandrelatedenzymesweredeterminedbyspectrophotometry.RESULTS:Comparedwiththecontrolgroup,themitochondrialrespiratorycontrolratio(RCR)declinedat6handremainedatalowleveluntilday7afterTBI(control,5.42±0.46;6h,5.20±0.18;12h,4.55±0.35;24h,3.75±0.22;2d,4.12±0.53;3d,3.45±0.41;7d,5.23±0.24,P<0.01).Thevalueofphosphate-to-oxygen(P/O)significantlydecreasedat12,24h,day2andday3,respectively(12h,3.30±0.10;24h,2.61±0.21;2d,2.95±0.18;3d,2.76±0.09,P<0.01)comparedwiththecontrolgroup(3.46±0.12).Twotroughsofmitochondrialrespiratoryfunctionwereseenat24handday3afterTBI.TheactivitiesofmitochondrialcomplexⅠ(6h:110±10,12h:115±12,24h:85±9,day2:80±15,day3:65±16,P<0.01)andcomplexⅡ(6h:105±8,12h:110±92,24h:80±10,day2:76±8,day3:68±12,P<0.01)wereincreasedat6hand12hfollowingTBI,andthensignificantlydecreasedat24h,day2andday3,respectively.However,therewerenodifferencesincomplexⅠandⅡactivitiesbetweenthecontrolandTBIgroups.Furthermore,pyruvatedehydrogenase(PDH)activitywassignificantlydecreasedat6handcontinuedupto7dafterTBIcomparedwiththecontrolgroup(6h:90±8,12h:85±10,24h:65±12,day2:60±9,day3:55±6,day7:88±11,P<0.01).Thechangesinα-ketoglutaricdehydrogenase(KGDH)activityweresimilartoPDH,exceptthatthedecreaseinKGDHactivitybeganat12hafterTBI(12h:90±12,24h:80±9,day2:76±15,day3:68±7,

简介：瞄准：调查影响他我有教养的老鼠小岛的生存能力和功能上的oxygenase-1(HO-1)基因转移在试管内。方法：小岛被管内胶原酶消化从Sprague-Dawley老鼠的胰孤立，并且由不连续的Ficoll密度坡度远心沉淀净化了。净化的老鼠小岛是有包含人的HO-1基因(Ad-HO-1)的adenoviral向量的transfected或提高了绿荧光灯的蛋白质基因(Ad-EGFP)，然后为七天有教养。Transfection被萤光显微镜检查和西方的污点证实。小岛生存能力被氮蒽orange/propidium碘化物评估荧光灯的染色。刺激葡萄糖的胰岛素版本用胰岛素放射性免疫测定工具包被检测并且被用来估计小岛的功能。刺激索引(SI)被在低葡萄糖刺激之上由胰岛素版本在高葡萄糖刺激之上划分胰岛素版本计算。结果：在七种天文化以后，有教养的老鼠小岛的生存能力显著地减少了(92%+/-6%对52%+/-13%，P<0.05)，并且刺激葡萄糖的胰岛素版本也显著地减少了(6.47+/-0.55mIU/L/30IEQ对4.57+/-0.40mIU/L/30IEQ，14.93+/-1.17mIU/L/30IEQ对9.63+/-0.71mIU/L/30IEQ，P<0.05)。有在20的MOI的adenoviral向量的老鼠小岛的Transfection是有效的，并且没损害小岛功能。在7dpost-transfection，Ad-HO-1transfected小岛的生存能力比控制小岛的高(71%+/-15%对52%+/-13%，P<0.05)。在Ad-HO-1transfected组之中在在低葡萄糖刺激(2.8mmol/L)之上的胰岛素版本没有有效差量，Ad-EGFPtransfected组织，并且控制组织P>0.05)，当时当由高葡萄糖(16.7mmol/L)刺激了时答案，在Ad-HO-1transfected组的胰岛素版本比在Ad-EGFP，transfected组织并且控制组显著地高，分别地(12.50+/-2.17mIU/L/30IEQ对8.87+/-0.65mIU/L/30IEQ；12.50+/-2.17mIU/L/30IEQ对9.63+/-0.71mIU/L/30IEQ，P<0.05)。Ad-HO-1transfected组的SI比Ad-EGFP，transfected组织并且控制组也显著地高，分

简介：AIMToexploretheprotectiveeffectsandunderlyingmechanismsoftotalpolysaccharidesoftheSijunzidecoction(TPSJ)ontheepithelialbarriersinvitro.METHODSCaco-2cellmonolayersweretreatedwithorwithoutTPSJinthepresenceorabsenceofTNF-α,andparacellularpermeabilityandtransepithelialelectricalresistance(TEER)weremeasuredtoevaluatetheepithelialbarrierfunction.Immunofluorescenceandwesternblottingwererespectivelyusedtoevaluatethedistributionandexpressionofthetightjunctionproteinsclaudin1,claudin2,zo3,andoccludininCaco-2cells.Westernblottingwasalsousedtoevaluatethecellularexpressionofmyosinlightchain(MLC),phosphorylatedMLC(pMLC),MLCkinase(MLCK),andnuclearfactor(NF)-κBp65.RESULTSTPSJpromotedtheproliferationofCaco-2cellsandinhibitedTNF-α-inducedsecretionofpro-inflammatorycytokines.Furthermore,TPSJsignificantlyamelioratedboththereductionofTEERandtheincreasedparacellularpermeabilityobservedintumornecrosisfactor(TNF)-α-damagedCaco-2monolayers.Furthermore,TPSJremarkablyattenuatedTNF-α-inducedmorphologicalchanges,downregulatedtheexpressionofclaudin1,claudin2,zo3,andoccludin,andmarkedlysuppressedTNF-α-mediatedupregulationofp-MLCandMLCKexpression.Finally,TPSJinhibitedtheactivationandexpressionofNF-κBp65.CONCLUSIONOurresultsdemonstratethatTPSJalleviatestheTNF-α-inducedimpairmentoftheintestinalepithelialcellbarrierfunctionbysuppressingNF-κBp65-mediatedphosphorylationofMLCKandMLC.