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简介:目的利用核糖核酸(RNA)干扰的方法,确定蛋白激酶Ca小干扰RNA(PKCαsiRNA)的体内最适作用浓度.探讨PKCαsiRNA对增生性玻璃体视网膜病变fPVR)防治作用。方法选择5~6周龄的C57BL/6j小鼠36只,通过玻璃体内注射分散酶诱导做成PVR小鼠模型,随机分为六组,每组6只小鼠,在1周后,5个治疗组的小鼠接受2肛lPKCαsiRNA的玻璃体腔注射.眼内终浓度分别为50nmol/L、100nmol/L、150nmol/L、200nmol/L、300nmol/L,而对应的阴性对照组接受的是2μlsiRNA,比较各组的PVR发生率;4周后取小鼠眼球用聚乙二醇和聚乙烯醇的混合物(OCT)包埋制作病理切片,进行苏木精一伊红(HE)染色,观察视网膜脱离情况。结果阴性对照组的PVR发生率为100%,50nmol/L浓度组PVR发生率为100%,100nmol/L浓度组、150nmol/L浓度组、200nmol/L浓度组PVR发生率都为66.67%。300nmol/L浓度组的PVR发生率为50.00%。不同浓度组的PVR发生率有差异,差异均有统计学意义(X^2=5.44,P〈0.05);HE染色结果显示阴性对照组和50nmol/L浓度组视网膜全部发生脱离,100~300nmol/IJ浓度组部分视网膜脱落.眼球结构基本完好。结论浓度为100~300nmol/LPKCαsiRNA通过玻璃体腔注射PKCαsiRNA对增生性玻璃体视网膜病变有一定的抑制作用。
简介:IntheapplicationofRNAitechnology,itisanessentialsteptodesignsiRNAapplicabletotargetgene.Atpresent,therearemanyresearchesandconclusionsonsiRNAdesign.ThispaperaimstotheinfluencesofmRNAsecondarystructureorsiRNAantisense-strandsecondarystructureonsiRNAsilenceefficiency.Thepaperalsodiscussestheproblemsandsetsoutfurtherinsightsintheresearch.
简介:SmallRNA(sRNA)-mediatedpost-transcriptionalregulationdiffersfromprotein-mediatedregulation.Throughbasepairing,sRNAcanregulatethetargetmRNAinacatalyticorstoichiometricmanner.Sometheoreticalmodelswerebuiltforcomparisonoftheprotein-mediatedandsRNA-mediatedmodesinthesteady-statebehaviorsandnoiseproperties.ManyexperimentsdemonstratedthatasinglesRNAcanregulateseveralmRNAs,whichcausescrosstalkbetweenthetargets.Here,wefocusonsomemodelsinwhichtwotargetmRNAsaresilencedbythesamesRNAtodiscusstheircrosstalkfeatures.Additionally,thesequence-functionrelationshipofsRNAanditsroleinthekineticprocessofbase-pairinghavebeenhighlightedinmodelbuilding.
简介:Longnon-codingRNAs(lncRNAs)refertoagroupofRNAsthatareusuallymorethan200nucleotidesandarenotinvolvedinproteingeneration.Instead,lncRNAsareinvolvedindifferentregulatoryprocesses,suchasregulationofgeneexpression.DifferentlncRNAsexistthroughoutthegenome.LncRNAsarealsoknownfortheirrolesindifferenthumandiseasessuchascancer.HOTAIRisanlncRNAthatplaysaroleasanoncogenicmoleculeindifferentcancercells,suchasbreast,gastric,colorectal,andcervicalcancercells.Therefore,HOTAIRexpressionlevelisapotentialbiomarkerfordiagnosticandtherapeuticpurposesinseveralcancers.ThisRNAtakespartinepigeneticregulationofgenesandplaysanimportantroleindifferentcellularpathwaysbyinteractingwithPolycombRepressiveComplex2(PRC2).Inthisreview,wedescribethemolecularfunctionandregulationofHOTAIRanditsroleindifferenttypesofcancers.