简介:AIM:TodiscusstheimpactofLyciumBarbarumPolysaccharide(LBP)andDanshensupurifiedfromTraditionalChineseMedicine(TCM)onvascularendothelialgrowthfactor(VEGF)ofrabbitswithretinalneovascularization.METHODS:Fortyrabbitsweredividedintonormalcontrolgroup,modelcontrolgroup,LBPgroupandDanshensugroup.Animalsinthenormalcontrolgroupwerefedinthenormaloxygenenvironment.Animalsintheotherthreegroupswereputintotheenvironmentwith70%oxygenfor5daysinordertobuildthemodelofoxygen-inducedvascularproliferationretinopathy.AndthendifferentTCMextractwasinjectedintotheabdominalcavitiesoftheseannimals.After7days,theVEGFcontentofintheserumofrabbitwasmeasuredbydoubleantibodysandwichmethod.RESULTS:DataanalysisindicatedthatVEGFcontentwasasfollows:Danshensugroupwaslowerthanmodelcontrolgroup(12.92±3.84ng/Lvs19.32±4.15ng/L,P<0.05);LBPgroupandnormalcontrolgroupwerelowerthanmodelcontrolgroup(12.92±3.84ng/L,9.26±1.61ng/Lvs19.32±4.15ng/L,P<0.01);totalbloodviscosity,plasmaviscosity,cholesterolcontent,fibrinogencontentandtriacylglycerolcontentafterperitonealinjectionofLBPandDanshensuwereobviouslylowerthanbeforeinjection.CONCLUSION:TCMextract-LBPandDanshensucanprominentlyreducethecontentofVEGFintheprocessofvascularproliferativeretinopathyofrabbit;canpreventtheoccurrenceofretinalmicrovasculardiseasebyimprovingpartialoxygen-deficientenvironmentoraffectingallkindsofnewgrowthfactor.
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。
简介:AIM:ExcessivedissolveofcornealtissueinducedbyMMPswhichwereactivatedbycytokinsandchemokineswillleadtocornealulcer.ThemolecularmechanismofLipoxinA4(LXA4)oncornealcollagendegradationinthreedimensionswasinvestigated.·METHODS:Rabbitcornealfibroblastswereharvestedandsuspendedinserum-freeMEM.TypeIcollagen,DMEM,collagenreconstitutionbufferandcornealfibroblastsuspensionweremixedonice.Theresultantmixturesolidifiedinanincubator,afterwhichtestreagentsandplasminogenwasoverlaidandthecultureswerereturnedtotheincubator.Thesupernatantsfromcollagengelincubationswerecollectedandtheamountofhydroxyprolineinthehydrolysatewasmeasured.ImmunoblotanalysisofMMP-1,-3andTMMP-1,-2wasperformed.MMP-2,-9wasdetectedbythemethodofGelatinzymography.Cytotoxicityassaywasmeasured.RESULTS:LXA4inhibitedcornealcollagendegradationinadoseandtimemanner.LXA4inhibitedtheIL-1βinducedincreasesinthepro-MMP-1,-2,-3,-9andactiveMMP-1,-2,-3,-9inaconcentrationdependentmanner.LXA4alsoinhibitedtheIL-1βinducedincreasesinTIMP-1,-2.CONCLUSION:Asapotentanti-inflammationreagent,LXA4caninhibitcornealcollagendegradationinducedbyIL-1βincornealfibroblaststhusinhibitingcornealdissolvingpathologyprocess.
简介:目的:使用Pentacam三维眼前段分析仪比较高度近视眼与正常人(正视眼)中央前房深度(centralanteriorchamberdepth,CACD)和前房角(anteriorchamberangle,ACA)两项前房参数差异,进一步了解高度近视眼的解剖学特点。方法:收集2010-10/2011-06在我院门诊就诊的正视眼82例,收集同期我院门诊与准分子激光中心就诊的高度近视眼68例,采用Pentacam三维眼前段分析仪测量CACD和ACA。对高度近视组与正视眼组的前房参数值进行两样本t检验,比较两组间参数有无差异。结果:Pentacam三维眼前段分析仪测得正常人CACD平均值为3.02±0.47mm,ACA平均值为33.26°±6.20°。高度近视眼的CACD平均值为3.24±0.38mm,ACA的平均值为39.55°±6.68°。高度近视眼与正视眼的两项前房参数值均存在显著性差异(均P〈0.05)。结论:Pentacam三维眼前段分析仪测量前房参数,高度近视眼与正视眼相比中央前房深度深、前房角宽。
简介:AIM:Tocomparethetrabecularmeshwork(TM)andirisapoptosisoftreatedanduntreatedprimaryopenangleglaucoma(POAG)patients.METHODS:Eighttreatment-naive,newlydiagnosed(group1)and11medlcaiytreated(group2)patientswithPOAGwereincludedinthestudy.Eachpatientunderwentalimbus-basedtrabeculectomy.TheTMandperipheralirisspecimensweredissectedoutandweresnap-frozeninliquidnitrogenandstoredat-80tuntiltheywereassayed.ApoptosisineachgroupwasassesedbyTUNELmethod.RESULTS:Themeanpatientagewas60.6±5.8years(53-68years)vs58.9±8.9years(47-70years)ingroup1andgroup2(P=0.859).Themeantreatmenttimeingroup2was22.2±7.3months(12-34months).ApoptoticindexesinTMandirisweresignificantlyhigherinPOAGpatientsusingmedication(group2)comparedtotreatment-naivePOAGpatients(group1)(P=0.004,0.015;respectively).CONCLUSION:LongtermadministrationoftopicalantiglaucomamedicationscausesadditionaltoxiceffectsonTM.