纳米氧化铈和氧化钇对小鼠原代成骨细胞增殖影响机制-mechanism of effect of nano cerium oxide and yttrium oxide on proliferation of primary osteoblasts in mice.docxVIP
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纳米氧化铈和氧化钇对小鼠原代成骨细胞增殖影响机制-mechanism of effect of nano cerium oxide and yttrium oxide on proliferation of primary osteoblasts in mice
摘要摘要本文研究了纳米氧化铈和氧化钇两种材料对小鼠原代成骨细胞增殖的影响机制。通过扫描电子显微镜、X射线衍射、动态光散射技术对纳米材料的理化性质进行了表征,以小鼠原代成骨细胞为模型,通过MTT实验检测了两种材料对细胞活力的影响。然后从细胞周期调控、细胞粘附力影响和清除活性氧自由基三个方面对纳米氧化铈促细胞增殖的机制进行了探讨;通过对细胞内活性氧、线粒体膜电位及细胞凋亡率的影响对纳米氧化钇抑制细胞增殖的机制进行了探讨,实验结论如下:1.两种尺寸的氧化铈纳米颗粒都能够促进小鼠原代成骨细胞增殖,其中30nm氧化铈促增殖效应高于60nm的氧化铈纳米颗粒。2.纳米氧化铈可以推动成骨细胞跨越G1/S期限制点,增加细胞进入S期数目,同时增加了成骨细胞的粘附力,从而促进细胞增殖。3.纳米氧化铈能够降低双氧水对成骨细胞造成的氧化损伤,且保护作用随纳米尺度减小而升高。纳米氧化铈可以提高模型细胞中超氧化物歧化酶和过氧化氢酶的活力,清除细胞中的活性氧,降低细胞凋亡率,从而缓解细胞的氧化损伤。4.纳米氧化钇抑制小鼠原代成骨细胞的增殖,抑制效果随尺度减小而增大,具有尺度依赖性。纳米氧化钇促进细胞内活性氧水平上升,引起细胞凋亡,从而抑制细胞的增殖。关键词氧化铈氧化钇成骨细胞增殖ⅠAbstractInthisarticle,themechanismsoftheceriumoxideandyttriumoxidenanoparticlesontheproliferationofprimaryosteoblastswerestudied.ThephysicalandchemicalpropertiesofnanomaterialswerecharacterizedbySEM,XRDandDLS.TheproliferationofosteoblastswasmeasuredbyMTTmethod.Thenthepromotionmechanismsofceriumoxidenanoparticlesontheproliferationofosteoblastswereinvestigatedfromcycleregulation,celladhesionandoxidativestress.Theinhibitionmechanismsofyttriumoxidenanoparticlesoncellproliferationwereresearchedthroughthechangeofintracellularreactiveoxygenspecieslevel,mitochondrialmembranepotentialandcellapoptosisrateofosteoblasts.Theresultsshowedthat:Ceriumoxidenanoparricleswithtwosizescanpromotetheproliferationoftheosteoblasts.Ceriumoxidenanoparricleswith30nmhaveahigherpromotioneffectthanthatof60nm.CeriumoxidenanoparriclescanstimulatemorecellstopassthroughtheG1/ScheckpointintoSphase,butdidnotchangethelengthofcellcycle.Furthermore,ceriumoxidenanoparticlescanalsoincreasetheadhesionofosteoblasts,thuspromotecellproliferation.Ceriumoxidenanoparriclescanrelievetheoxidationdamageinducedbyhydrogenperoxide.Theprotectiveeffectswereincreasedwiththedecreasingsizeofnanoparticles.Ceriumoxidenanoparticlesprotectosteoblastsagainsthydrogenperoxideinducedoxidativedamage,suppressionofantioxidantenzymesdepletionandcellapoptosisviaitsreactiveoxidativespeciesscavengingmechanism.Yttriumoxidenanoparriclescaninhibittheproliferationoftheosteoblastsandtheinhibitioneffectwasincreasedwiththed
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