理肠四方对溃疡性结肠炎大鼠结肠组织TNF-αmRNA表达

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WorldChinJDigestol2004March;12(3):706-710ISSN1009-3079CN14-1260/RPOBox2345Beijing100023,ChinaFax:+86-10-85381893Email:wcjd@wjgnet.com•BASICRESEARCH•αEffectofChineseherbcompoundsLichangsifangonTNF-αmRNAexpres-sionofcolontissueinratswithulcer-ativecolitisMing-YiQiu,HengFan,Jia-JunMei,Guan-XinShen,Song-LinLiu,Ying-QianZhaoMing-YiQiu,Jia-JunMei,Song-LinLiu,Ying-QianZhao,HubeiCollegeofTraditionalChineseMedicine,Wuhan430061,HubeiProvince,ChinaHengFan,DepartmentofIntegratedTraditionalandWesternMedicine,XieheHospital,TongjiMedicalCollege,HuazhongUniversityofSci-enceandTechnology,Wuhan430022,HubeiProvince,ChinaGuan-XinShen,XieheHospital,TongjiMedicalCollege,HuazhongUni-versityofScienceandTechnology,Wuhan430022,HubeiProvince,ChinaSupportedbyHubeiProvincialDepartmentofEducation,No.99Z014Correspondenceto:Ming-YiQiu,HubeiCollegeofTraditionalChi-neseMedicine,1Tanhualin,Wuchang430061,HubeiProvince,China.qiumingyi9256@163.comReceived:2003-06-06Accepted:2003-07-30AbstractAIM:TostudytheeffectofLichangsifang(LCSF)onTNF-αmRNAexpressioninratswithulcerativecolitis(UC).METHODS:Ninty-eightSDratswererandomlydividedintosevengroups,andeverygrouphadfourteenrats(sevenratsweremale,andseven,female),namelythenormalcontrolgroup,thepathologiccontrolgroup,solfasalazine(SASP)group,Wumeiwan(WMW)group,Baitouwengtang(BTWT)group,Senglingbaishusan(SLSS)groupandTongxieyaofang(TXYF)group.Exceptthenormalcontrolgroup,theothersixanimalmodelgroupsofUCweremadethroughtheintegrationofgeneralimmunityandlocalstimu-lationwithDNCBandaceticacid.ThesixanimalmodelgroupsofUCweretreatedbySASP,TXYF,WMW,BTWT,SLBSSandTXYFrespectively.Afterthesetreatment,thechangesofsomeimmuneindexesinthecolontissuesuchastheleverofTNF-αmRNAexpressionwereevaluatedbyinsituhybridization.RESULTS:ThelevelofTNF-αmRNAexpressioninpatho-logicgroupswassignificantlyhigherthanthatinnormalcontrols(P0.01,t=4.128vsnormalcontrol),TheTNF-αmRNAexpressionwasdecreasedinWMWthanthoseinotherpathologicgroups(P0.01,t=3.435orP0.05t=2.593).TNF-αmRNAexpressionwasdecreasedinWMWgroupthanthoseinBTWTgroup,SLBSSgroupandTXYFgroup(P0.05,q=2.581vsBTWTgroup,q=2.834vsSLBSSgroup,q=2.624vsTXYFgroup).TherewasnoremarkabledifferenceintheleverofTNF-αmRNAexpressionamongBTWTgroup,SLBSSgroupandTXYFgroup(P0.05).CONCLUSION:ThismodelinducedwithDNCBandaceticacidissuccessful.Itisobviousthatthecytokinesplayimpor-tantrolesinpathogenesisofUC,especiallyproinflammtorycytokinesFNF-α,whichcanpromoteinflammation.WMWisthemosteffectiveamongthecompounds,whichhavecura-tiveeffectsbyadjustingimmunityandinhibitingabnormalinflammatoryreactioninthecourseofUC.QiuMY,FanH,MeiJJ,ShenGX,LiuSL,ZhaoYQ.EffectofChineseherbcompoundsLichangsifangonTNF-αmRNAexpressionofcolontissueinratswithulcerativecolitis.ShijieHuarenXiaohuaZazhi2004;12(3):706-710ααααααααααα±±nα707αα±n×708ISSN1009-3079CN14-1260/RABCDEFGα×ααααααα709ABCDEFGαακ12000;8:336-33722001;9:1431-143432001;9:698-70142002;10:916-92152002;10:865-8666α2001;17:216-21871999;7:381-38381999;7:786-78792001;25:47-5110ZhengL,GaoZQ,WangSX.Achroniculcerativecolitismodelinrats.WorldJGastroenterol2000;6:150-15211PadolI,HuangJQ,HogaboamCM,HuntRH.TherapeuticeffectsoftheendothelinreceptorantagonistRo48-5695intheTNBS/DNBSratmodelofcolitis.EurJGastroenterolHepatol2001;12:257-26512TjandraK,LeT,SwainMG.Exaperimentalcolitisattenuatesdevelopmentoftoxin-inducedcholangitisinrats.DigDisSci2002;47:1216-122313LiuZ,GeboesK,ColpaertS,D’HaensGR,RutgeertsP,CeuppensJL.IL-15ishighlyexpressedininflammatoryboweldiseaseandregulateslocalTcell-dependentcytokineproduction.JImmunol2000;164:3608-361514κ2002;41:252-255710ISSN1009-3079CN14-1260/R••...(ISI)(JCR):WorldJournalofGastroenterologyWJG20022.5321535.WJG20024513SCI5876797.WJG20011.445722;WJG20000.993327.1998(ASPPDF)PubMedPubMedWJG.

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