Objective:Toobservetheeffectofglucagon-likepeptide-1(GLP-1)ontheexpressionofPar-4/NF-κBandtheapoptosisofisletβcellsindiabeticmice.Methods:Experimentalmicewererandomlydividedintonormalcontrolgroup(Cgroup),Par-4knockoutgroup(CPgroup),diabetesgroup(Dgroup),diabetesandPar-4knockoutgroup(DPgroup),GLP-1+diabetesgroup(GDgroup),andGLP-1+diabetesandPar-4knockoutgroup(GDPgroup),with8miceineachgroup.Foreachgroup,theapoptosisrateofisletβcellswasdeterminedbyTUNELassay,theproteinexpressionlevelsofPar-4andNF-κBweredeterminedbyWesternblot,andinsulinsecretionwasmeasuredbyELISA.Results:TherewerenosignificantdifferencesbetweentheCPgroupandtheCgroupintheapoptosisrateofisletβcells(P=0.965),NF-κBexpression(P=0.754),andinsulinsecretion(P=0.797).ComparedwiththeCgroupandCPgroup,theDgrouphadsignificantlyincreasedapoptosisrate(P=0.000)andexpressionofPar-4(P=0.000)andNF-κB(P=0.000),butsignificantlyreducedinsulinsecretion(P=0.000).ComparedwiththeDgroup,theDPgroupandGDgrouphadsignifi-cantlydecreasedapoptosisrate(P=0.000,P=0.000)andexpressionofPar-4(P=0.000,P=0.000)andNF-?资B(P=0.000,P=0.002),butsignificantlyimprovedinsulinsecretion(P=0.000,P=0.026).ComparedwiththeGDgroup,theGDPgrouphadsignificantlydecreasedapoptosisrate(P=0.000)andexpressionofPar-4(P=0.000)andNF-κB(P=0.015),butsignificantlyimprovedinsulinsecretion(P=0.026).TherewerenosignificantdifferencesbetweentheDPgroupandtheGDPgroupintheapoptosisrateofisletβcells(P=0.930),theexpressionofPar-4(P=0.965)andNF-κB(P=0.875),andinsulinsecretion(P=0.797).Conclusion:GLP-1improvestheapoptosisofisletβcellsandinsulinsecretionintype2diabetesbyinhibitingtheexpressionofPar-4/NF-κB.
LeiXiaotian, ZhengYanling, GanXiaguang, LengWeiling, ZhangLing, ChenBing, WuQinan. GLP-1improvestheapoptosisofisletβcellsintype2diabetesviathePar-4/NF-κBpathway[J]. Journal of Chongqing Medical University,2020,45(3):319-