简介：Thispaperaimstotheresearchoftheimpactoffluidshearstressontheadhesionbetweenvascularendothelialcellsandleukocyteinducedbytumornecrosisfactor-α(TNF-α)bymicrofliudicchiptechnology.Microfluidicchipwasfabricatedbysoftlithograph;Endothelialmicrofluidicchipwasconstructedbyoptimizingtypesoftheextracellularmatrixproteinsmodifiedinthemicrochannelandcellincubationtime;humanumbilicalveinendothelialcellsEA.Hy926linedinthemicrochannelwereexposedtofluidshearstressof1.68dynes/cm~2and8.4dynes/cm~2respectively.Meanwhile,adhesionbetweenEA.Hy926cellsandleukocytewasinducedbyTNF-αunderaflowcondition.EA.Hy926cellculturedinthestaticconditionwasusedascontrolgroup.Thenumbersoffluorescently-labeledleukocyteinmicrochannelwerecountedtoquantizetheadhesionlevelbetweenEA.Hy926cellsandleukocyte;cellimmunofluorescencetechniquewasusedtodetecttheintercellularadhesionmolecule(ICAM-1)expression.TheconstructedendothelialmicrofluidicchipcanaffordtothefluidshearstressandrespondtoexogenousstimulusofTNF-α;comparedwiththeadhesionnumbersofleukocyteincontrolgroup,adhesionbetweenEA.Hy926cellsexposedtolowfluidshearstressandleukocytewasreducedunderthestimulusofTNF-αataconcentrationof10ng/ml(P<0.05);leukocyteadhesionwithEA.Hy926cellsexposedtohighfluidshearstresswasreducedsignificantlythanEA.Hy926cellsincontrolgroupandEA.1Hy926cellsexposedtolowfluidshearstress(P<0.01);theregulationmechanismoffluidshearstresstotheadhesionbetweenEA.Hy926cellsandleukocyteinducedbyTNF-αwasthroughthewayofICAM-1.Theendothelialmicrofluidicchipfabricatedinthispapercouldbeusedtostudythefunctionsofendothelialcellinvitroandprovideanewtechnicalplatformforexploringthepathophysiologyoftherelatedcardiovascularsystemdiseasesunderaflowenvironment.