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：目的：探讨Avastin与Lucentis对人脐静脉血管内皮细胞（humanumbilicalveinendothelialcells，HUVEC）增殖和迁移的影响，了解其抑制血管生成的途径。方法：采用MTT比色法研究相同浓度Avastin与Lucentis对HUVEC增殖作用的差异；Transwell小室检测相同浓度Avastin与Lucentis对HUVEC迁移作用的差异。结果：MTT比色法显示，各浓度Avastin组、Lucentis组与对照组相比，吸光度值具有统计学差异（P〈0．05），相同浓度Avastin组与Lucentis组吸光度值无统计学差异（P〉0．05）；Transwell分析方法显示，各浓度Avastin组、Lucentis组与对照组相比，HUVEC迁移率具有统计学差异（P〈0．05），相同浓度Avastin组与Lucentis组HUVEC细胞迁移率无统计学差异（P〉0．05）。结论：Avastin与Lueentis均可以抑制HUVEC增殖和迁移：随着药物浓度增加，对HUVEC增殖和迁移的抑制作用增强；相同浓度Avastin与Lucentis在体外实验中对HUVEC增殖和迁移的抑制作用无统计学差异（P〉0．05）。

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：观察多西环素对碱烧伤大鼠角膜炎症细胞浸润的抑制作用。方法：健康SD大鼠32只，随机分为对照组、多西环素组，每组16只大鼠。建立角膜碱烧伤模型后，多西环素组予3g／L多西环素眼液点眼，对照组予眼液溶媒点眼。分别于碱烧伤后第3，7，14，21d观察计算炎症指数，角膜取材后进行病理切片及炎症细胞计数，行ICAM-1的ELISA检测。结果：多西环素组各时间点结膜充血、角膜水肿较对照组轻，炎症指数均明显低于对照组，差异有统计学意义（P〈0．05）。多西环素组各时间点炎症细胞计数少于对照组（P〈0．05）。多西环素组各时间点大鼠角膜的ICAM-1表达低于对照组（P〈0．05）。结论：多西环素可以抑制碱烧伤大鼠角膜的炎症细胞浸润，其机制可能是抑制ICAM-1的表达。

简介：AIM:ToinvestigatetheroleofRho-associatedproteinkinase(ROCK)inhibitor,Y27632,inmediatingtheproductionofextracellularmatrix(ECM)componentsincludingfibronectin,matrixmetallo-proteinase-2(MMP-2)andtypeIcollagenasinducedbyconnectivetissuegrowthfactor(CTGF)ortransforminggrowthfactor-β(TGF-β)inahumanretinalpigmentepithelialcellline,ARPE-19.METHODS:TheeffectofY27632ontheCTGForTGF-βinducedphenotypeinARPE-19cellswasmeasuredwithimmunocytochemistryasthechangeinF-actin.ARPE-19cellsweretreatedwithCTGF(1,10,100ng/mL)andTGF-β(10ng/mL)inserumfreemedia,andanalyzedforfibronectin,laminin,andMMP-2andtypeIcollagenbyRT-qPCRandimmunocytochemistry.CellswerealsopretreatedwithanROCKinhibitor,Y27632,toanalyzethesignalingcontributingtoECMproduction.·RESULTS:TreatmentofARPE-19cellsinculturewithTGF-βorCTGFinducedanECMchangefromacobblestonemorphologytoamoreelongatedswirlpatternindicatingamesenchymalphenotype.RT-qPCRanalysisanddifferentgeneexpressionanalysisdemonstratedanupregulationinexpressionofgenesassociatedwithcytoskeletalstructureandmotility.CTGForTGF-βsignificantlyincreasedexpressionoffibronectinmRNA(P=0.006,P=0.003respectively),lamininmRNA(P=0.006,P=0.005),MMP-2mRNA(P=0.006,P=0.001),COL1A1mRNA(P=0.001,P=0.001),COL1A2mRNA(P=0.001,P=0.001).PreincubationofARPE-19withY27632(10mmol/L)significantlypreventedCTGForTGF-βinducedfibronectin(P=0.005,P=0.003respectively),MMP-2(P=0.003,P=0.002),COL1A1(P=0.006,P=0.003),andCOL1A2(P=0.006,P=0.004)geneexpression,butnotlaminin(P=0.375,P=0.516).CONCLUSION:OurstudydemonstratedthatbothTGF-βandCTGFupregulatetheexpressionofECMcomponentsincludingfibronectin,laminin,MMP-2andtypeIcollagenbyactivatingtheRhoA/ROCKsignalingpathway.Duringthisprocess,ARPE-19cellswereshowntochangefromanepithelialtoamesenchymalphenotypeinvi