vegf expression and cell apoptosis in nod mouse retina

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1、VEGFexpressionandcellapoptosisinNODmouseretina×÷ÕߣºCaiª²RuiLi,Shuª²GuangSun¡¾ÕªÒª¡¿Toinvestigateretinalvascularendothelialgrowthfactor(VEGF)levelandretinalcellsapoptosisintheearlystageofdiabeticNODmouseretina.METHODS:Animalsweredividedintothecontrolgroup(nonª²diabetesmice)(2,4,6,8,12wee

2、ksgroup,n=30)anddiabetesgroup(2,4,6,8,12weeksgroup,n=30).ELISA(Enzymeª²LinkedImmunosorbentAssay)wasperformedtodetectVEGFlevelinbothserumandretina.Transmissionelectronmicroscopemethodwasusedtoexamineretinalcellapoptosis.¤rRESULTS:Comparedwiththecontrolgroup,VEGFlevelsinserumandretinawerei

3、ncreasedsignificantlyintheNODgroup(12weeks:4.9¡À0.4¦Ìg/gversus0.19¡À0.1¦Ìg/ginserumsample,P<0.01;165.0¡À9.0¦Ìg/gversus18.0¡À4.0¦Ìg/ginretinalsample,P<0.01).ThereexistsapositivecorrelationbetweenserumVEGFandretinalVEGFlevelsintheearlydiabeticNODmice(¦Ã=0.9902,P=0.001).Thenumberofthe

4、cellsapoptosisintheganglioncellsandendotheliumcanalsobeenfoundincreasedsignificantlyintheNODgroup(P<0.01).CONCLUSION:ThehighVEGFexpressionmaybe14contributedtoincreaseretinalcellsapoptosis.ManyfactorsassociatedwithretinalVEGFexpressionmightinvolveintheearlydiabetesstage.¡¾¹Ø¼ü´Ê¡¿retin

5、a;apoptosis;vascularendotheliumgrowthfactor;NODmiceINTRODUCTION¡¡¡¡Diabeticretinopathyisthemostcommondiabeticeyediseaseandaleadingcauseofblindness.Diabeticretinopathyischaracterizedincreasedmicrovascularpermeabiª²lity,celldamage,abnormalbloodflowautoregulation,disorderedangiogenesisandin

6、creasedadhesivepropertiesoftheendothelium.Allthesefactorscancausecapillaryocclusion,microvasculardegenerationandabnormalneovasª²cularization,theneventuallyleadingtoirreversibleblindness.Hyperglycemiaisanindependentriskfactorforthedevelopª²mentofcardiovasculardisease[1].However,themechani

7、smsofhyperglycemiaandhyperglycemia¬ðseffectontissuedamageandclinicalcomplicationsremainunclear.Vascularendothelialgrowthfactor(VEGF)mightplaya14particularlyimportantroleindiabeticretinopathy[2].TheexpressionchangesandeffectofVEGFonapoptosisinretinalcellsinducedbyhyperglyc