PI3kAkt信号通路在周期性张应力介导的牙周膜成纤维细胞凋亡中的作用的开题报告Title：TheRoleofPI3kAktSignalingPathwayinPeriodontalLigamentFibroblastApoptosisMediatedbyCyclicalTensileStressBackground：Periodontitisisacommondiseaseindentalclinic,whichiscausedbychronicinflammationofperiodontaltissues,leadingtothedestructionofperiodontalsupportingtissuesandinevitablyresultintoothloss.Periodontalligamentfibroblasts(PDLFs)arethemaincellsinperiodontaltissuesandplayacentralroleinmaintainingthehomeostasisofperiodontaltissues.Periodontaltissuesareunderconstantmechanicalstressfromchewingandspeaking,whichmaycontributetothedevelopmentofperiodontitis.However,theunderlyingmechanismofhowmechanicalstressaffectsPDLFsandcontributestoperiodontitisremainslargelyunclear.Objectives：ToinvestigatetheroleofPI3kAktsignalingpathwayincyclicaltensilestress-inducedPDLFapoptosis,andtodeterminethepotentialtherapeutictargetforperiodontitis.Methods：CyclicaltensilestresswillbeappliedtoPDLFcellsbyusingacustom-madedevicefor12hours.TheexpressionlevelofPI3kAktsignalingpathwaymarkers,includingp-Akt,p-PI3K,Bax,andBcl-2,willbemeasuredbyWesternblotandRT-PCRaftercellswereexposedtocyclicaltensilestress.Meanwhile,theapoptosisrateofPDLFwillbedetectedbyflowcytometryandTUNELstaining.Additionally,thePDLFwillbetreatedwithPI3kAktsignalingpathwayinhibitortoexplorewhethertheinhibitionofPI3kAktcanattenuatethecyclicaltensilestress-inducedapoptosis.ExpectedResults：OurresearchisexpectedtorevealthemechanismofcyclicaltensilestressonPDLFsapoptosisandtofindnewtherapeutictargetsforperiodontitis.Theresultsofthisstudywillimproveourunderstandingofperiodontitisandprovidesupportfornoveltherapeuticapproachesforthepreventionandtreatmentofperiodontitis.