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探讨在椎间盘退变期间细胞自噬对丝裂原活化蛋白激酶(MEK)、细胞信号调节激酶(ERK)、转录因子CNC-bZIP蛋白(NRF1)、自噬相关蛋白7(Atg7)表达的影响.[方法]选取腰椎间盘严重变性达到Pfirrmann5级的患者18例(观察组)与年轻腰椎骨折患者18例(对照组)作为研究对象,取腰椎间盘组织分离单个髓核细胞,流式细胞仪分选CD24阳性细胞.在模拟生理压力环境下培养细胞96h,应用RT-PCR法测定髓核细胞中MEK、ERK、NRF1及Atg7mRNA的表达,Westernblot方法检测髓核细胞中MEK、ERK、NRF1及Atg7蛋白水平的表达.[结果]RT-PCR结果显示:观察组 MEK、ERK、NRF1及Atg7 mRNA的表达水平显著高于对照组,差异均有统计学意义(P<0.05);Westernblot结果显示:观察组 MEK、ERK、NRF1及Atg7蛋白的表达显著高于对照组,差异有显著统计学意义(P<0.05).[结论]在椎间盘退变期间细胞自噬可上调髓核细胞 MEK、ERK、NRF1及Atg7蛋白的表达,MEK、ERK、NRF1、Atg7信号通路是调控髓核细胞凋亡的主要信号传导途径,可能参与腰椎退行性变的发病过程.“,”Toinvestigatetheautophagyofmitogen-activatedproteinkinase(MEK),cellsig-nal-regulatedkinase(ERK),transcriptionfactorCNC-bZIPprotein(NRF1)andautophagy-associatedprotein 7 (Atg7)duringintervertebraldiscdegenerationtoexplorethebasicresearchandclinicaltreatmentoflumbar degenerativechanges.[Methods]Atotalof18patientswithseveredegenerationoflumbarintervertebraldisc (Pfirrmanngrade5)intheobservationgroupand18patientswithyounglumbarvertebraefracturesinthe controlgroupwereselectedasthestudysubjects.Thenucleuspulposuscellswereisolatedfromlumbarinter-vertebraldisctissueandCD24positivecellsweresortedbyflowcytometry.Thecellswereculturedfor96h undersimulatedphysiologicalpressure.TheexpressionsofMEK,ERK,NRF1andAtg7 mRNAinnucleus pulposuscellsweredetectedbyRT-PCR.ThelevelsofMEK,ERK,NRF1andAtg7proteininnucleuspulpo-suscellsweredetectedby Westernblot.[Results]ResultsofRT-PCRshowedthattheexpressionlevelsof MEK,ERK,NRF1andAtg7mRNAintheobservationgroupweresignificantlyhigherthanthoseinthecon-trolgroupt(P<0.05).WesternblotresultsshowedthattheexpressionlevelsofMEK,ERK,NRF1and Atg7proteinsintheobservationgroupwerehigherthanthoseinthecontrolgroup.Thedifferencesbetween thetwogroupswerestatisticallysignificant(P<0.05).[Conclusion]Autophagyupregulatestheexpressionof MEK,ERK,NRF1andAtg7proteinsinnucleuspulposuscellsduringdegenerationofintervertebraldisc.The MEK/ERK/NRF1/Atg7signalingpathwayisthemainsignalingpathwayregulatingnucleuspulposuscellap-optosisandmaybeinvolvedinthepathogenesisoflumbardegenerativechanges.