Background:InvestigatingtheinfluenceonatherosclerosisofhyperglycemiarabbitbyG-CSFmaygivereferenceforclinicapplication.Methods:30NewZeelandhealthymalerabbitsweredividedinto4groupsrandomly,whosebloodwasdrewfromtheearveinweeklytotestthechangeofTC、TG、HDL、LDL.Aftersacrifice,theaortathoracicaliswastakentomaketheSudaneseIIIfatdye,conventionalHEdyeaswellasscanningelectronmicroscopetoobservetheformchangeofendothelialcells,grueltypemottlingandfatfoam..IHCofMMP9andTIMP2wasusedtoexploratethematrix,andmanydataofpathologywerecalculatedbyLeicaQwinV3imageanalysissystem,meanwhileRT-PCRandWBwereimpliedtoconfirmit.Results:Fedwithhighfatfood,thelevelofbloodfatsuchasTC,LDLandsooncanrisetopeakin6weeks,thengodowntostableplatformperiodafter8weeks.G-CSFcanmakethefatcurveappeardouble-peak,andthestatisticsdifferenceofTC,LDLarrives2weeksearlier,contrasttothecontrolgroup(P<0.05).ButithadnoeffectonTG.AddingG-CSFtoordinaryfedgroupcanmakethosebloodfathavesomefluctuationbutcan’tgetthesignificantdeviation.TheanalysisbypathologyalsofoundG-CSFcanincreasetheplaquearea,endomembranethickness,andtheexpressofMMP9/TIMP2.TheWBandRT-PCRofMMP/TIMPalsosupporttheformerresultofIHC.Thescanselectronmicroscopefoundthefragmentsofendothelialcellincreasesobviouslywhenatherosclerosisappeared,shrinksinshape,sothesamepointwascertificated.Conclusion:G-CSFhascertaineffectontheendothelialcellshape,andstimulatethebloodfatslevel,primarilyTC,LDL.Forthisreasonitcanaggravateatherosclerosis.ThemechanismmayberelatetomatrixbecauseofthechangeinMMP/TIMPfamily.
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