简介：目的：通过对比姜黄素与Avastin抑制大鼠碱烧伤后角膜新生血管（cornealneovascularization,CNV）及血管内皮生长因子（vascularendothelialgrowthfactor,VEGF）表达水平的影响,进一步探讨姜黄素抑制CNV形成的机制。方法：选取SD大白鼠共30只,建立碱烧伤模型,随机将大鼠分成A,B两组,各15只,A组中右眼为实验组A1组,左眼为空白对照组A2;B组中右眼为实验组B1,左眼为空白对照组B2。A1组给予40μmol/L姜黄素配置成的滴眼液,A2组滴用生理盐水;B1组给予5g/LAvastin滴眼液,B2组滴用生理盐水。根据不同时间点取角膜组织进行病理切片研究、抽取房水进行ELISA测定,计算出每视野计数微新生血管及房水中VEGF含量。对以上指标进行对比分析研究。结果：两种药物均未发现在角膜水肿、角膜修复等方面的毒副作用。对新生血管的影响,两种药物CNV计数均明显低于空白对照组（P〈0.01）,两种药物之间对新生血管影响的对照,平均CNV计数无显著性区别。A1组与A2组对比、B1组与B2组对比,实验组VEGF均明显低于对照组,有高度显著性统计学意义（P〈0.01）,A1组与B1组对照,平均VEGF含量A1组高于B1组,有统计学意义（P〈0.05）。结论：姜黄素的VEGF抑制能力可能不如Avastin,但在整体抗CNV的能力上并不输于Avastin,说明姜黄素还参与了干预角膜碱烧伤CNV形成的其他机制。

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.