简介:AIM:Toexaminetheexpressionofsurvivinandvascularendothelialgrowthfactor(VEGF)duringthedevelopmentofretinalneovascularization(NV)inamousemodel.·METHODS:Awell-characterizedmurinemodelofretinalNVwasusedtostudytheexpressionofsurvivinandVEGF.NVoftheretinawasinducedinmicebyexposureto75%O2frompostnataldayP7toP12,followedbyreturntoroomairfromP12toP17.ExpressionofsurvivinandVEGFproteinwasanalyzedbyImmunohistochemistry.Inaddition,mousemodelofproliferativeretinopathywasanalyzedbyretinalfluoresceinangiographyandquantificationanalysis.·RESULTS:Thenormalmicehadbothsuperfiekalanddeepvascularlayersthatextendedfromtheopticnervetotheperiphery.Inintraocularpressure(IOP)micewerecharacterizedbyrepresentatypicalpatternofpathologicalretinalNV.Therearelessorlittlenucleiofnewvesselsvascularendothelialcellbreakingthroughtheinnerretinalthaninretinopathyofprematurity(ROP)mice,largeclustersofbloodvesselswereadherenttotheinternallimitingmembrane(ILM)(0.27±0.20vs23.38±1.027,t=9.454,P<0.001).DuringtheangiogenicperiodfromP13toP17,survivinandVEGFproteinexpressionincreasedinexperimentalretinascomparedwithcontrolsamples(2.56±0.46vs3.34±0.40,t=17.43,P<0.01:2.18±0.75vs4.34±0.25,t=19.61,P<0.01).ProteinlevelsofVEGFandsurvivnhassignificantlypositivecorrelation(P<0.05,r=0.411).·CONCLUSION:CorrelationwasmadeattheproteinlevelsofsurvivinexpressioncomparedwiththatofVEGFinamurinemodelofretinalNV,whichsuggestsatemporalroleforsurvivinandVEGFinnewvesselformationinresponsetohypoxicstimulation.
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:瞄准:在微容器密度(MVD)和脉管的内皮生长的表情调查差别,并且在MVD之中探索关联在前列腺癌症(PCa)之间的因素(VEGF),VEGF-C和VEGFreceptor-3(VEGFR-3)纸巾和邻近的良性的纸巾,Jewett-Whitmore阶段,格利森分数和在PCa的前进的VEGF,VEGF-C和VEGFR-3的表情。方法:免疫组织化学的途径被采用在癌症区域和71个主要职业人员静电干扰腺癌标本的外部良性的区域检测CD34,VEGF,VEGF-C和VEGFR-3的表情。统计分析然后被执行根据试验性并且诊所数据。结果:都显著地与邻近的良性的上皮(P<0.01)相比在恶意的上皮/癌症房间在VEGF,VEGF-C和VEGFR-3的调整表情上面被发现。当在肿瘤区域(P<0.01)比较VEGF-C或VEGFR-3的表示时,在阶段D的病人在阶段A,B或C比病人有一个显著地更高的分数。另外,重要关联在Jewett-Whitmore阶段和VEGF-C之间被观察(r=0.738,P<0.01),临床的阶段和VEGFR-3(r=0.410,P<0.01),VEGF-C和格利森分数(r=0.401,P<0.01),VEGFR-3和格利森分数(r=0.581,P<0.001)并且MVD和VEGF(r=0.492,P<0.001)。结论:VEGF和VEGF-C的增加的表情仔细与PCa的前进被联系。为PCa前进的增加的VEGF表示的主要贡献到过起来调整MVD,它维持了肿瘤织物的生长优点。然而,VEGF-C和VEGFR-3的增加的表情的主要角色是提高lymphangiogenesis并且提供一条主要小径让癌症房间传播。
简介:Radiotherapy,astandardadjuvanttosurgery,improvessurvivalratesinpatients,butresistancetotreatmentbysomegliomaslimitsthesuccessofclinicalapplication.Emergingevidenceindicatesthatthetumormicroenvironmentcontributestoradiationresistancebyregulatingthelevelsofcytokinesandgrowthfactors[1;2].
简介:目的观察生长抑素对大鼠移植性肝癌血管内皮生长因子(VEGF)、基质金属蛋白酶-1(MMP-1)表达的影响,初步探讨生长抑素抑制大鼠移植性肝癌生长的机理。方法制作大鼠移植性肝癌的动物模型,随机分为2组,对照组(n=11),治疗组(n=8)。治疗组腹腔注射善宁每天100μg/kg,分2次注射,对照组注射等量生理盐水。10d后心脏采血0.5ml,后处死大鼠,大鼠血液室温下4h,待其凝固,离心(3000转/min)10min,分离血清放入-80℃冰箱保存。酶联免疫吸附试验检测血清VEGF,原位杂交法检测瘤组织VEGF、MMP表达。结果治疗组血清VEGF值低于对照组,瘤组织VEGFmRNA、MMP-1mRNA在对照组、治疗组中均有阳性表达,而治疗组表达水平较对照组低(P<0.05)。结论:生长抑素抑制血清VEGF,转移相关基因VEGF、MMP-1表达降低,可能是生长抑素抑制大鼠移植性肝癌生长的机理之一。
简介:Adultstem/progenitorcellsplayimportantrolesintissuehomeostasisandhaveimportantimplicationsforregenerativemedicine.Itwasoncethoughtthatformationofnewbloodvesselsinadultonlyoccursthroughangiogenesis,aprocesswherebynewvesselsareformedfromexistingmatureendothelialcells;whilevasculogenesis,wherenewvesselsarederivedfromdifferentiationofendothelialprogenitorcells(EPCs),wasthoughttooccurexclusivelyinembryos.ThediscoveryofadultEPCsafewyearsagohaschangedthisoldparadigm;andsubsequentstudiesshowedthatEPCsmaybeapromisingtoolforthetreatmentofvasculardisorders.However,therehavebeenconflictingreportsonsubtypes,surfacemarkers,andfunctionsofEPCs;andthustheexactoriginandidentityofEPCsremaintobedefined.AcommonapproachtoobtainEPCsistoisolateandculturemononuclearcellsfromperipheralbloodandtoselectadherentcellsfor
简介:摘要糖尿病性视网膜病变(diabeticretinopathy,DR)是糖尿病最常见和最严重的微血管并发症之一。现研究发现该病已成为当今中老年以上人群致盲的首要原因。其基本病理改变是血-视网膜屏障破坏、新生血管形成、血管膜收缩、牵拉视网膜脱离。研究证实,血管内皮生长因子(VEGF)在DR引起管腔狭窄和血液改变,以及促进DR后期发生视网膜缺氧、缺血和新生血管的形成。VEGF作为与DR联系最为紧密的细胞因子,在整个过程中起着重要的调节作用;而VEGF的表达受到胰岛素水平、甘糖酯等多种因素影响。本文对影响DR中VEGF表达的各种相关因素进行系统性综述,旨在为DR的相关药物治疗提供思路。
简介:目的:探讨生长激素(growthhormone,GH)对实验大鼠牙齿移动过程中血管内皮生长因子(vascularendothelialgrowthfactor,VEGF)在牙周组织中表达的影响方法:将40只7周龄大的雄性Wistar大鼠根据是否注射生长激素分为实验组(E)和对照组(C)。将50g力值加于近中左侧上颌第一磨牙:E组和C组分别腹部皮下注射GH(0.15IU/公斤/天)及等剂量的生理盐水:大鼠分别在第1、3、7、14和21天处死。上颌第一磨牙及其牙周组织切片行VEGF免疫组织化学染色,并进行图像分析和统计:结果:无论张力侧及压力侧VEGF在实验组表达的量均高于对照组,第3天组中张力侧及压力侧实验组平均光密度值分别为174.47土7.53和345.80+25.46与其各自对照组相比较数据具有统计学意义(P<0.05),两侧实验组的VEGF的表达强度峰值均出现在第7天,分别为669.97+3.22和923.77+18.41差异具有统计学意义(P
简介:摘要卵泡发育可分为原始卵泡、生长卵泡和成熟卵泡3个阶段,其中生长卵泡阶段又可分为窦前卵泡、窦卵泡及排卵前卵泡。卵泡发育过程受到来自卵母细胞、颗粒细胞、膜细胞、基质、血管等多方的因素相互作用,变化丰富、复杂,过程中任何一分子或信号通路的异常即有可能引起卵泡发育的障碍。本文就影响生长卵泡发育阶段的相关因素进行梳理与总结。
简介:Marsdeniaetenacissimaeextract(MTE),commonlyknownasXiao-Ai-PinginChina,isatraditionalChineseherbmedicinecapableofinhibitingproliferationandmetastasisandboostingapoptosisinvariouscancercells.However,littleisknownaboutthecontributionofMTEtowardstumorangiogenesisandtheunderlyingmechanism.ThepresentstudyaimedtoevaluatetheeffectsofMTEontheproliferationandapoptosisofhumanumbilicalveinendothelialcells(HUVECs)andthemolecularism.3-(4,5-dimethylthiazol-2-yl)-5(3-carboxymethoxyphenyl)-2-(4-sulfopheny)-2H-tetrazolium,innersalt(MTS)andPI-stainedflowcytometryassaysrevealedthatMTEdose-dependentlyreducedtheproliferationofHUVECsbyarrestingcellcycleatSphase(P<0.05).AnnexinV-FITC/PI-stainedflowcytometryconfirmedthatMTE(160μL·mL-1)enhancedtheapoptosisofHUVECssignificantly(P<0.001).Real-timequantitativeRT-PCRandWesternblotanalysesshowedanincreaseinBaxexpressionandasharplydeclineinBcl-2expression;caspase-3wasactivatedsimultaneouslyinadose-dependentmanner(P<0.05).Furtherstudyobservedthedose-dependentdown-regulationofvascularendothelialgrowthfactor(VEGF)receptor-2(VEGFR-2),P2Y6receptor(P2Y6R),andchemokine(C-Cmotif)ligand2(CCL-2),alongwiththeactivationofPKCδandup-regulationofp53inadose-dependentmannerinMTE-treatedselectedcells(P<0.05).Collectively,theresultsfromthepresentstudysuggestedthatMTEsuppressedtheproliferationbyattenuatingCCL-2-mediatedVEGF/VEGFR2interactionsandpromotedtheapoptosisthroughPKCδ-inducedp53-dependentmitochondrialpathwayinHUVECs,supportingthatMTEmaybedevelopedasapotentanti-cancermedicine.
简介:摘要目的分析脉管癌栓与其他临床病理因素的关系及其对胃癌预后的影响。方法回顾性分析621例胃癌患者的临床病理资料,根据患者是否存在脉管癌栓将其分为脉管癌栓阳性组和脉管癌栓阴性组。比较两组胃癌患者5年累积生存率的差异,分析脉管癌栓与其他临床病理因素的关系及其对胃癌预后的影响。结果621例胃癌患者中,脉管癌栓发生率为31.7%(197例),二分类Logistic回归分析显示,肿瘤的分化程度、浸润深度、淋巴结转移是发生胃癌脉管癌栓的独立影响因素(P<0.01)。趋势χ2检验显示,肿瘤的分化程度、浸润深度、淋巴结转移与胃癌脉管癌栓阳性率呈线性相关关系(P<0.01),其中淋巴结转移与脉管癌栓的相关性更显著(r=0.387)。单因素分析显示,脉管癌栓阳性组术后5年累积生存率显著低于脉管癌栓阴性组,差异有统计学意义(46.7% vs 73.3%,P<0.01)。多因素分析显示,年龄、肿瘤直径、TNM分期、脉管癌栓是影响胃癌患者预后的独立危险因素(P均<0.05)。进一步分层分析显示,在Ⅲ期胃癌患者中脉管癌栓阳性组5年累积生存率低于脉管癌栓阴性组,差异有统计学意义(36.1% vs 51.4%;P<0.05)。结论脉管癌栓是影响胃癌患者预后的独立危险因素,结合脉管癌栓与TNM分期可更好地判断胃癌患者的预后,指导更合理的治疗。
简介:AbstractFluid resuscitation is an essential intervention in critically ill patients, and its ultimate goal is to restore tissue perfusion. Critical illnesses are often accompanied by glycocalyx degradation caused by inflammatory reactions, hypoperfusion, shock, and so forth, leading to disturbed microcirculatory perfusion and organ dysfunction. Therefore, maintaining or even restoring the glycocalyx integrity may be of high priority in the therapeutic strategy. Like drugs, however, different resuscitation fluids may have beneficial or harmful effects on the integrity of the glycocalyx. The purpose of this article is to review the effects of different resuscitation fluids on the glycocalyx. Many animal studies have shown that normal saline might be associated with glycocalyx degradation, but clinical studies have not confirmed this finding. Hydroxyethyl starch (HES), rather than other synthetic colloids, may restore the glycocalyx. However, the use of HES also leads to serious adverse events such as acute kidney injury and bleeding tendencies. Some studies have suggested that albumin may restore the glycocalyx, whereas others have suggested that balanced crystalloids might aggravate glycocalyx degradation. Notably, most studies did not correct the effects of the infusion rate or fluid volume; therefore, the results of using balanced crystalloids remain unclear. Moreover, mainly animal studies have suggested that plasma may protect and restore glycocalyx integrity, and this still requires confirmation by high-quality clinical studies.
简介:目的探讨重组人类肝细胞生长因子(rhHGF)对胶质瘤细胞增殖及血管内皮生长因子(VEGF)表达的影响。方法用5、10、20、30μg/L不同浓度的rhHGF作用于体外培养的U251胶质瘤细胞并设立空白对照组,甲基噻唑基四唑(MTT)法检测细胞增殖;免疫组化及Westernblot检测增殖细胞核抗原(PCNA)和VEGF表达。结果与对照组相比,rhHGF明显促进U251细胞的增殖和生长,其作用呈时间效应关系和一定浓度范围内的剂量效应关系(P〈0.05)。Westernblot及免疫组化检测显示,20μg/LrhHGF作用后U251细胞PCNA和VEGF表达上升,呈时间依赖性(P〈0.05);细胞外调节蛋白激酶(ERK)抑制剂PD98059呈剂量依赖性抑制rhHGF诱导的PCNA和VEGF表达增加。结论rhHGF可能通过ERK信号途径促进胶质瘤细胞增殖和VEGF表达,从而影响胶质瘤的生长和血管发生。