简介：瞄准：估计probioticBifidobacteriumlactis的反煽动性的效果(B。lactis)在大肠炎的一个采纳转移模型。方法：施主和接受者老鼠收到了任何一个B。lactis或象在在天真、规章的T房间的混合的转移以前喝水一个星期直到牺牲的控制(deManRogosaSharpe)中等的细菌的文化。结果：所有接受者老鼠开发了结肠的发炎的符号，但是重量损失的重要减小在B被观察。与控制鼠标相比的喂lactis的接受者鼠标。而且，向mucosal厚度和稀释上皮的损坏的减少的一个趋势被揭示。支持inflammatory和T房间标记的结肠的表示显著地在B被减少。与控制相比的喂lactis的接受者老鼠。附随地，forkhead盒子蛋白质3，规章的T房间的一个标记，由B是显著地起来调整的。lactis。结论：B的每天口头的管理。lactis对煽动性的还原剂和T房间调停人有能力，在一只老鼠的特定的标记大肠炎当模特儿支持规章的T房间。

简介：Hepaticencephalopathy(HE)isasevereneuropsychiatricsyndromethatmostcommonlyoccursindecompensatedlivercirrhosisandincorporatesaspectrumofmanifestationsthatrangesfrommildcognitiveimpairmenttocoma.AlthoughtheetiologyofHEisnotcompletelyunderstood,itisbelievedthatmultipleunderlyingmechanismsareinvolvedinthepathogenesisofHE,andoneofthemainfactorsisthoughttobeammonia;however,theammoniahypothesisinthepathogenesisofHEisincomplete.Recently,ithasbeenincreasinglydemonstratedthatinflammation,includingsystemicinflammation,neuroinflammationandendotoxemia,actsinconcertwithammoniainthepathogenesisofHEincirrhoticpatients.Meanwhile,agoodnumberofstudieshavefoundthatcurrenttherapiesforHE,suchaslactulose,rifaximin,probioticsandthemolecularadsorbentrecirculatingsystem,couldinhibitdifferenttypesofinflammation,therebyimprovingtheneuropsychiatricmanifestationsandpreventingtheprogressionofHEincirrhoticpatients.TheantiinflammatoryeffectsofthesecurrenttherapiesprovideanoveltherapeuticapproachforcirrhoticpatientswithHE.ThepurposeofthisreviewistodescribetheinflammatorymechanismsbehindtheetiologyofHEincirrhosisanddiscussthecurrenttherapiesthattargettheinflammatorypathogenesisofHE.

简介：AIM.Toinvestigatetheeffectofpyrrolidinedithiocarbamate(PDTC),anovelnuclearfactor-κB(NF-κB)inhibitor,onexpressionofmultipleinflammatorymediatorsandneutrophilicinflammationofcoldpreservedgraftsafterratlivertransplantationanditssignificance.METHODS:Orthotopiclivertransplantation(OLT)wasperformedafter24hofcoldstorageusingUniversityofWisconsinsolutionwithvariedconcentrationsofPDTC.WedeterminedthetimecourseofNF-κBactivationandexpressionofmultipleinflammatorysignals,suchastumornecrosisfactor-α(TNF-α),cytokine-inducibleneutrophilchemoattractant(CINC),andintercellularadhesionmolecule-1(ICAM-1)byELISAmethods.Serumalanineaminotransferase(ALT),intrahepaticmyeloperoxidase(MPO)/WBC(ameasureofneutrophilaccumulation)andMac-1expression(ameasureofcirculatingneutrophilactivity)werealsoevaluated.RESULTS:PDTCdecreasedNF-κBactivationinducedbyprolongedcoldpreservationinadosedependentmanner(from20mmol/Lto60mmol/L),diminishedTNF-α,CINC,ICAM-1proteinsinthegrafts,andreducedtheexpressionfincreasesinplasmaTNF-αlevelsinducedbyprolongedoldpreservation.NeutrophilicinflammationofthegraftwassignificantlysuppressedafterpreservationwithPDTC(P<0.05).ThetotalneutrophilaccumulationinPDTC(40mmol/L)group(7.04±0.97)wasmarkedlyreducedcomparedtocontrolgroup(14.07±1.31)(P<0.05).Mac-1expressionwassignificantlyreducedinPDTC(40retool/L)group(181±11.3%)comparedwiththecontrolgroup(281±13.2%)(P<0.05)at6hafterreperfusion.Furthermore,PDTCinhibitedtheincreasedserumALTlevelsafterlivertransplantation.CONCLUSION:PDTCcaninhibitBNF-κBactivationandexpressionoftheinflammatorymediators,whichareassociatedwithimprovedgraftviabilityviainhibitingintrahepaticneutrophilicinflammation.OurstudysuggeststhatatherapeuticstrategydirectedatinhibitionofNF-κBactivationinthetransplantedlivermightbeeffectiveinreducing