简介：在细胞的增长和内长的脉管的endothelial生长因素(VEGF)上调查melatonin的效果的目的在胰腺的癌房间(PANC-1)的表示。方法PANC-1房间为这研究是有教养的。在文化媒介的分泌VEGF集中用ELISA方法被决定，在肿瘤房间的VEGF生产被immunocytochemistry，和VEGFmRNA表示检测被RT-PCR决定。更高结果melatonin集中显著地禁止了细胞的增长，与展出最高禁止的效果的1mmol/L集中(P<0.01)。在房间文化上层清液和intra小房的VEGF集中都显著地在melatonin(1mmol/L)以后被减少孵化(P<0.05)。VEGFmRNA表示在观察时期期间以一种时间依赖者方式显著地减少了(P<0.05)。结论高melatonin集中显著地禁止了胰腺的癌房间的增长。内长的VEGF表示被melatonin孵化也压制。

简介：Objective:Toexploretheprobabilityofvascularendothelialgrowthfactor(VEGF)antisenseoligodeoxynucleotidesasadevelopingnewtherapeuticstrategyforglioma.Methods:VEGFproteinexpressionwasdetectedbyS-Pimmunohistochemicaltechnique.TumorcellapoptosiswasobservedbyTUNELmethod.Results:Comparedwithcontrol,VEGFproteinexpressionwasinhibitedbyantisenseoligodeoxynucleotidesinvitro.Andtheinhibitoryeffectsincreasedwiththeincreasingconcentration.VEGFpositiveratewas82.10%incontrolgroup,whilein2.5,5,10(mol/LAODNgroups,theywere70.00%,57.85%,53.20%respectively.Noinhibitioneffectwasfoundinthecelllinestreatedwithmissenseandsenseoligodeoxynucleotides.Invivo,antisenseoligodeoxy-nucleotidestherapyalsoinhibitedVEGFproteinexpressionandinducedtheincreaseofapoptotictumorcells.However,ithasnoeffectontumorcellproliferation.Conclusion:ItishopefulthatVEGFantisenseoligodeoxynucleotidesmaybeanewgenetherapymethodtogliomathroughitsantiangiogenesiseffectbyinhibitionofVEGF.

简介：Objective:Toanalyzetheexpressionofinduciblenitricoxidesynthase(iNOS),endothelialnitricoxidesynthase(eNOS)andvascularendothelialgrowthfactor(VEGF)inhepatocellularcarcinoma(HCC)anditsrelationtoangiogenesis.Methods:Tissuesectionsfrom71HCCpatientswereexaminedimmunohistochemicallyforproteinexpressionofiNOS,eNOS,andVEGF.Microvessaldensity(MVD)wascountedbyendothelialcellsimmunostainedbyanti-CD34antibody.Results:PositiveimmunostainingforiNOS,eNOSwasdetectedin83.1%and85.9%ofHCCrespectively.INOSandeNOSwerenotdetectedinnormalhepatictissue.MVDwas34.3±1.5/HPand38.6±1.6/HPinHCCwithpositivestainingforiNOSandVEGFwhileitwas31.2±2.8/HP,and22.4±2.0/HPinHCCwithnegativestainingforiNOSandVEGF(P<0.01).AcorrelationbetweenNOSexpressionandVEGFinHCCwasnotobserved.Conclusion:iNOSandeNOSmayplayaroleinmalignanttransformationfpost-hepaticcirrhosis.TheexpressionofiNOSandVEGFfavorsangiogenesisofHCC.