简介:目的:探讨miR-181在白内障晶状体组织中的表达情况,及其对人晶状体上皮细胞凋亡的调控机制。方法:利用Realtimeq-PCR方法,检测年龄相关性白内障患者晶状体前囊膜和人晶状体上皮细胞凋亡模型中miR-181的表达情况;利用Lipofectamine2000瞬时转染miR-181mimic和inhibitor调节人晶状体上皮细胞中miR-181的表达,利用Realtimeq-PCR方法验证转染效率,利用流式细胞仪检测细胞凋亡率的变化。结果:与对照组相比,年龄相关性白内障患者晶状体前囊膜组和人晶状体上皮细胞凋亡模型组,miR-181的表达显著升高;miR-181mimic转染组,miR-181的表达显著升高,细胞凋亡率显著升高;miR-181inhibitor转染组,miR-181的表达显著降低,细胞凋亡率显著降低,差异均有统计学意义(P〈0.01)。结论:miR-181在年龄相关性白内障晶状体组织中呈高表达,miR-181能够促进人晶状体上皮细胞凋亡,从而可能在年龄相关性白内障的发病过程中发挥一定作用,miR-181可能成为白内障非手术治疗的一种新途径,但具体机制有待进一步研究。
简介:AIM:TocomprehensivelyevaluatethepotentialassociationofCOL1A1polymorphismswithhighmyopiabyasystematicreviewandMeta-analysis.METHODS:AllassociationstudiesonCOL1A1andhighmyopiareporteduptoJune10,2014inPubMed,Embase,WebofScience,andtheChineseBiomedicalDatabasewereretrieved.Oddsratios(ORs)and95%confidenceintervals(95%CIs)wereanalyzedforsinglenucleotidepolymorphisms(SNPs)usingfixed-andrandom-effectsmodelsaccordingtobetween-studyheterogeneity.PublicationbiasanalyseswereconductedbyEgger’stest.RESULTS:Atotaloffourstudiesfromreportedpaperswereincludedinthisanalysis.TheMeta-analysesforCOL1A1rs2075555,composedof2304highmyopiapatientsand2272controls,failedtodetectanysignificantassociationwithhighmyopia.Atotalof971casesand649controlsweretestedforCOL1A1rs2269336.TheassociationofCOL1A1rs2269336withhighmyopiawasobservedinrecessivemodel(CCvsCG+GG,P=0.03)andinheterozygousmodel(CGvsGG,P=0.04),butnotinothermodels.CONCLUSION:ThisMeta-analysisshowsthatCOL1A1rs2269336(CCvsCG+GG)affectsindividualsusceptibilitytohighmyopia,whereasthereisnoassociationdetectedbetweenSNPsrs2075555andhighmyopia.Giventhelimitedsamplesize,furtherinvestigationsincludingmoreethnicgroupsarerequiredtovalidatetheassociation.
简介:目的:探讨线粒体膜电位(△ψm)、Caspase3在As2O3诱导ACC-2细胞凋亡中的作用。方法:进行ACC-2细胞培养,将As2O3建立不同药物浓度梯度(0,1.0,2.0,4.0,8.0μmol/L)分别作用于ACC-2细胞,用Rh123染色,流式细胞仪检测8.0μmol/LAs2O3作用前、后(24h),ACC-2细胞的线粒体膜电位(△ψm)变化;用多功能酶标仪进行Caspase3活性检测。结果:空白对照组ACC-2细胞内Rh123荧光强度最强,8.0μmol/LAs2O3处理组ACC-2细胞内Rh123荧光强度减弱,其差异有显著性(P〈0.05);随着As2O3药物浓度的增高(0,1,2,4,8μmol/L),ACC-2细胞的Caspase3酶活力单位逐渐增加。结论:As2O3作用于ACC-2细胞,可通过降低线粒体膜电位从而引起细胞凋亡。随着As2O3药物浓度的增高,ACC-2细胞的Caspase3酶活力单位逐渐增加,Caspase3被激活,细胞可发生不可逆转的凋亡过程。