rack1与nfκb信号通路相关蛋白在幽门螺杆菌感染相关胃黏膜病变中的表达-expression of rack 1 and nf κ b signaling pathway related proteins in gastric mucosal lesions associated with helicobacter pylori infection.docxVIP
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rack1与nfκb信号通路相关蛋白在幽门螺杆菌感染相关胃黏膜病变中的表达-expression of rack 1 and nf κ b signaling pathway related proteins in gastric mucosal lesions associated with helicobacter pylori infection
摘要κBα蛋白表达高于慢性非萎缩性胃炎组,有显著差异(40%vs77.5%,p0.01)。(3)与Hp感染的关系:将慢性非萎缩性胃炎组、癌前病变组各自分为Hp阳性和阴性组,进行组间比较。结果显示在胃黏膜病变早期阶段,Hp阳性组RACK1显著高于Hp阴性组,差异有统计学意义(100%vs90%;87.5vs90%,p0.05),而Hp阳性和阴性组间IκBα与p-IκBα蛋白表达无显著性差异(p0.05)。(4)胃癌组织中RACK1与IκBα、p-IκBα表达的关系:胃癌组织中RACK1与IκBα蛋白表达正相关(p0.01),与p-IκBα负相关,差异均有统计学差异(p0.01)。2.Hp作用GES-1后RACK1与NF-κB信号通路相关蛋白表达情况Hp活菌(MOI=50:1)作用GES-1细胞后,RACK1表达量在作用后30min开始升高,3h达到高峰(p0.01),6h开始下降(p0.05)。NF-κB信号通路相关蛋白中p65表达无明显变化(p0.05),而p-p65(Ser276)蛋白表达水平在各时间点均明显升高,30min开始升高,3h达到高峰(p0.01),6h内均高于0h(p0.05),p-p65(Ser536)表达水平在3h显著升高(p0.01),作用6h时仍高于0h(p0.05),结论:1.RACK1表达下调和NF-κB信号通路活化可能参与了胃黏膜癌变过程。2.Hp感染相关胃粘膜癌变早期RACK1表达上调,这是否参与了Hp相关胃黏膜癌变发生尚待进一步探讨。关键词:胃粘膜癌变;幽门螺杆菌;RACK1;NF-κBABSTRACTBackgroundandAim:Gastriccanceristhefifthmostcommonmalignanttumorintheworld,leadingtothethirdtumorassociateddeath,nearlyonemillionnewcasesincreasingperyear.Seventypercentofthefinancialburdenfallsinthedevelopingcountries,especiallyinAsia.Hpinfectionisthemainriskfactorofgastriccancer.AlargenumberofresearcheshavedemonstratedthatHpplaysimportantrolesintheinitiationandtheprogressionofthegastricmucosalcancerationtheprocessofwhichincludethechronicatrophicgastritis,intestinalmetaplasia,dysplasiaandgastriccancer.However,theunderlyingmechanismofHpinfectioningastriccancerstillremainsunclear.MostrelatedstudiesrevealedthattheNF-κBsignalpathwayisactivatedaftertheinfectionofHp,whichsubsequentlyiscloselyrelatedwiththegastritis,gasriculcerandtheincidence,development,survivalandprognosisofgastriccancer.NF-κBisanimportantmultifunctionalnucleartranscriptionfactor.Intherestingstate,theNF-κBdimerp50/p65combineswiththeinhibitoryproteinsIκBtoformacomplexandexsitinthecytoplasminaninactivatedstate.ManyextracellularstimulileadtothephosphorylationofIκBproteinsandpromotetheirubiquitinationandsubsequentdegradationbyproteasome.Thisprocessleadstothetranslocationofp65fromthecytoplasmtothenucleus,whereitinitiatesthetranscriptionofaseriesoftargetgenes.Thenitplaysanimportantroleintheinflammation、immunityandtumor.Therefore,itmayprovidene
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