摘要
AIMToinvestigatetheeffectoffenugreeklactone（FL）onpalmitate（PA）-inducedapoptosisanddysfunctionininsulinsecretioninpancreaticNIT-1β-cells.METHODS：CellswereculturedinthepresenceorabsenceofFLandPA（0.25mmol/L）for48h.Then,lipiddropletsinNIT-1cellswereobservedbyoilredOstaining,andtheintracellulartriglyceridecontentwasmeasuredbycolorimetricassay.Theinsulincontentinthesupernatantwasdeterminedusinganinsulinradioimmunoassay.Oxidativestress-associatedparameters,includingtotalsuperoxidedismutase,glutathioneperoxidaseandcatalaseactivityandmalondialdehydelevelsinthesuspensionswerealsoexamined.Theexpressionofupstreamregulatorsofoxidativestress,suchasproteinkinaseC-α（PKC-α）,phospho-PKC-αandP47phox,weredeterminedbyWesternblotanalysisandreal-timePCR.Inaddition,apoptosiswasevaluatedinNIT-1cellsbyflowcytometryassaysandcaspase-3viabilityassays.RESULTS：Ourresultsindicatedthatcomparedtothecontrolgroup,PAinducedanincreaseinlipidaccumulationandapoptosisandadecreaseininsulinsecretioninNIT-1cells.OxidativestressinNIT-1cellswasactivatedafter48hofexposuretoPA.However,FLreversedtheabovechanges.TheseeffectswereaccompaniedbytheinhibitionofPKC-α,phospho-PKC-αandP47phoxexpressionandtheactivationofcaspase-3.CONCLUSION：FLattenuatesPA-inducedapoptosisandinsulinsecretiondysfunctioninNIT-1pancreaticβ-cells.Themechanismforthisactionmaybeassociatedwithimprovementsinlevelsofoxidativestress.
出版日期
2015年12月22日（中国期刊网平台首次上网日期，不代表论文的发表时间）
