简介：AIM:Toestablishtheratmodelofstreptozotocin(STZ)induceddiabeticretinopathy(DR),whichisthemostcommoncauseofvisuallossandblindnessinpatientswithdiabetes,andobservethegeneexpressionofvascularendothelialgrowthfactor(VEGF)anditsreceptorsduringthedevelopmentofDR.METHODS:AratmodelofdiabeteswasestablishedbyintraperitonealinjectionofSTZ.Thediabeticratswerehousedfor2,3and4monthsafterthedevelopmentofdiabetes.Retinalhistopathologicalobservationwasperformed.TheretinalvesselswereobservedbyimmunofluorescencestainingbyCD31.ThemRNAexpressionofVEGF,VEGFreceptor1and2(VEGFR1/2)inratretinawasdetectedbyreversetranscriptionpolymerasechainreaction(RT-PCR)analysis.RESULTS:Retinalhistopathologicalobservationshowedthemorphologicalchangesofinnernuclearlayer(INL)andouternuclearlayer(ONL)atanytime-point,andalsodemonstratedtheincreasednewvesselsatboth3,4monthsafterthedevelopmentofdiabetes.TheCD31stainingresultsshowedthatthenumberofvesselswasincreasedintheretinasofdiabeticratsatboth3and4monthsafterthedevelopmentofdiabetes.Ascomparedtothenormalrats,themRNAexpressionofVEGFwasincreasedinretinasofdiabeticratsat3monthsafterthedevelopmentofdiabetes,whileVEGFR1andVEGFR2mRNAexpressionwasincreasedat2,3and4monthsafterthedevelopmentofdiabetes.CONCLUSION:Takentogether,ourresultsdemonstratedthatDRwasoccurredat3monthsafterthedevelopmentofdiabetes,andthemRNAexpressionofVEGF,VEGFR1andVEGFR2wereincreasedintheprocessofDR.ThepresentstudyfurtherevidencedtheinvolvementofVEGFanditsreceptorsintheprocessofDR.