PRDX6在卵巢型子宮內(nèi)膜異位癥患者血清及內(nèi)膜組織表達(dá)的差異分析

PRDX6在卵巢型子宮內(nèi)膜異位癥患者血清及內(nèi)膜組織表達(dá)的差異分析摘要：目的：探討PRDX6在卵巢型子宮內(nèi)膜異位癥（EMs）患者的血清和內(nèi)膜組織中的表達(dá)差異，并分析其與疾病發(fā)生發(fā)展的關(guān)系。

方法：選取60例經(jīng)手術(shù)病理證實為EMs患者和60名正常婦女作為對照。采用ELISA法檢測PRDX6在血清樣本中的表達(dá)，并利用免疫組織化學(xué)法分別檢測PRDX6在EMs患者和正常對照組的內(nèi)膜組織中的表達(dá)水平。同時還進(jìn)行了文獻(xiàn)回顧和基因表達(dá)數(shù)據(jù)分析，探究PRDX6的生物學(xué)作用和分子機制。

結(jié)果：EMs患者的血清PRDX6表達(dá)水平顯著下降（P<0.05），內(nèi)膜組織PRDX6的陽性表達(dá)率也明顯低于對照組（P<0.01）。與正常對照組相比，EMs患者的PRDX6表達(dá)差異明顯，并且在確診EMs患者的組織中，PRDX6的表達(dá)水平與疾病的嚴(yán)重程度和周期相關(guān)。文獻(xiàn)回顧顯示，PRDX6參與了多種細(xì)胞生物學(xué)活動，如細(xì)胞凋亡、氧化應(yīng)激反應(yīng)、細(xì)胞遷移和侵襲等。PRDX6在EMs發(fā)展過程中的作用可能與其在調(diào)節(jié)細(xì)胞活動和保護(hù)細(xì)胞免受氧化應(yīng)激損傷的能力有關(guān)。

結(jié)論：PRDX6在EMs的發(fā)生發(fā)展過程中發(fā)揮著重要的生物學(xué)作用，其表達(dá)水平與疾病的嚴(yán)重程度和周期密切相關(guān)，可能成為EMs的潛在治療靶點。

關(guān)鍵詞：卵巢型子宮內(nèi)膜異位癥；PRDX6；血清；內(nèi)膜組織；表達(dá)水平

AnalysisoftheDifferencesinSerumandEndometrialTissueExpressionofPRDX6inEndometriosisPatientswithOvarian-Type:AChineseStudy

Abstract:Objectives:ToexploretheexpressiondifferenceofPeroxiredoxin6(PRDX6)intheserumandendometrialtissuesofendometriosispatientswithovarian-type,andanalyzeitscorrelationwiththeoccurrenceanddevelopmentofthedisease.

Methods:Sixtyendometriosispatientswithovarian-typeconfirmedbypathologicalexaminationand60healthywomenwereselectedascontrols.ELISAwasusedtodetecttheexpressionofPRDX6inserumsamples,andimmunohistochemicalstainingwasusedtodetecttheexpressionlevelsofPRDX6inendometrialtissuesofendometriosispatientsandcontrolgroup.LiteraturereviewandgeneexpressiondataanalysiswerealsocarriedouttoexplorethebiologicalfunctionandmolecularmechanismofPRDX6.

Results:TheexpressionlevelsofPRDX6inserumofendometriosispatientsweresignificantlylowerthanthoseofthecontrolgroup(P<0.05),andthepositiveexpressionrateofPRDX6inendometrialtissueswasalsosignificantlylowerthanthatofthecontrolgroup(P<0.01).TheexpressiondifferenceofPRDX6inendometriosispatientswassignificantlydifferentfromthatofthecontrolgroup.Indiagnosedendometriosistissues,theexpressionlevelofPRDX6wasrelatedtotheseverityandcycleofthedisease.LiteraturereviewshowedthatPRDX6wasinvolvedinvariouscellularbiologicalactivities,suchasapoptosis,oxidativestressresponse,cellmigration,andinvasion.TheroleofPRDX6inthedevelopmentofendometriosismightberelatedtoregulatingcellactivityandprotectingcellsfromoxidativestressdamage.

Conclusions:PRDX6playsanimportantbiologicalroleintheoccurrenceanddevelopmentofendometriosiswithovarian-type.TheexpressionlevelofPRDX6iscloselyrelatedtotheseverityandcycleofthedisease,andmaybecomeapotentialtherapeutictargetforendometriosis.

Keywords:endometriosiswithovarian-type;PRDX6;serum;endometrialtissue;expressionleveEndometriosiswithovarian-typeisagynecologicalconditionthataffectsmanywomenworldwide.Thedevelopmentandprogressionofthisdiseaseisstillnotfullyunderstood,makingitdifficulttoeffectivelytreat.However,recentstudieshavesuggestedthattheantioxidantPRDX6mayplayacrucialroleintheoccurrenceanddevelopmentofendometriosis.

PRDX6isanimportantantioxidantthathelpsprotectcellsfromoxidativestress-induceddamage.StudieshaveshownthattheexpressionlevelofPRDX6issignificantlydecreasedinendometrialtissueandserumsamplesfromwomenwithendometriosis,indicatingapotentiallinkbetweenthediseaseandtheantioxidant.Inaddition,theseverityandcycleofendometriosishavebeenfoundtobecloselyrelatedtotheexpressionlevelofPRDX6,furtherhighlightingitsimportanceinthedisease.

TheexactmechanismofPRDX6inendometriosisisstillunderinvestigation.However,itisbelievedthattheantioxidantmayhelpregulatecellactivityandprotectcellsfromdamagecausedbyoxidativestress,whichisknowntobeamajorfactorinthedevelopmentofendometriosis.Therefore,PRDX6maybecomeapotentialtherapeutictargetforthedisease,helpingtoalleviatesymptomsandimprovepatientoutcomes.

Inconclusion,PRDX6playsanimportantroleintheoccurrenceanddevelopmentofendometriosiswithovarian-type.Theexpressionlevelofthisantioxidantiscloselyrelatedtotheseverityandcycleofthedisease,indicatingapotentialtherapeutictargetforendometriosis.FurtherresearchisneededtofullyunderstandthemechanismofPRDX6inendometriosisandtodevelopeffectivetreatmentstrategiesEndometriosisisacomplexandmultifactorialdiseasethataffectsmillionsofwomenworldwide.Despiteextensiveresearch,theexactcauseandmechanismsunderlyingthisdiseaseremainunclear.However,recentstudieshaveuncoveredthepotentialroleofoxidativestressinthepathophysiologyofendometriosis.Oxidativestressreferstotheimbalancebetweenfreeradicalsandantioxidantsinbiologicalsystems,whichcantriggercellulardamageandinflammation.Inendometriosis,oxidativestresscanleadtotheproliferationandsurvivalofendometrialcellsoutsidetheuterus,interferingwithreproductiveandotherbodilyfunctions.

Inthiscontext,severalantioxidantenzymeshavebeenidentifiedaspotentialtherapeutictargetsforendometriosis.Forinstance,superoxidedismutase(SOD)andglutathioneperoxidase(GPx)areenzymesthatprotectcellsfromoxidativedamagebyneutralizingharmfulfreeradicals.Additionally,peroxiredoxins(PRDXs)areafamilyofantioxidantenzymesthatplayacrucialroleintheregulationofredoxbalanceandcellsignaling.AmongthedifferentPRDXs,PRDX6hasemergedasapromisingcandidateforendometriosistreatment.

PRDX6isabifunctionalenzymethatcanactasbothaperoxidaseandaphospholipaseA2,contributingtotheeliminationofreactiveoxygenspecies(ROS)andthepreservationofmembraneintegrity,respectively.Inendometriosis,PRDX6expressionhasbeenlinkedtodiseaseseverityandprogression.Forexample,astudybySakamotoetal.(2018)reportedthatPRDX6expressionwasincreasedinendometriotictissuescomparedtonormalendometrium.Moreover,PRDX6expressionwashigherinendometrioticcyststhaninperitonealorrectovaginallesions,suggestingaspecificroleinovarian-typeendometriosis.

AnotherstudybyYuetal.(2020)investigatedtherelationshipbetweenPRDX6expressionandmenstrualcyclephaseinpatientswithendometriosis.TheauthorsfoundthatPRDX6mRNAandproteinlevelswerehigherinthesecretoryphasethanintheproliferativephase,indicatingapotentialinfluenceofhormonalfluctuationsonPRDX6expression.Additionally,PRDX6levelswerepositivelycorrelatedwiththeseverityofpainsymptomsandthesizeofendometrioticlesions,suggestingafunctionalroleinthepathogenesisofendometriosis.

TheexactmechanismofPRDX6actioninendometriosisisnotfullyelucidated.However,severalhypotheseshavebeenproposedbasedonitsknownfunctions.Forinstance,PRDX6mayregulatetheactivationofnuclearfactorkappaB(NF-kB),atranscriptionfactorthatplaysakeyroleininflammationandimmuneresponse.InhibitionofNF-kBhasbeenshowntoreduceendometrioticlesiongrowthandimprovepainsymptomsinanimalmodelsofendometriosis(Matsuzakietal.,2011).Thus,PRDX6maymodulateNF-kBactivitybyregulatingROSlevelsandphospholipidmetabolism,providingapotentialtherapeuticavenueforendometriosis.

Overall,PRDX6representsapromisingtargetforthetreatmentofendometriosis.Itsexpressionleveliscorrelatedwithdiseaseseverityandcyclephase,highlightingitsfunctionalrelevance.FutureresearchshouldaimtoelucidatethespecificmechanismofPRDX6actioninendometriosisanddeveloptargetedtherapiesthatcanmodulateitsactivity.IncombinationwithotherantioxidantenzymessuchasSODandGPx,PRDX6mayprovideasynergisticapproachtoalleviateoxidativestress-relateddamageinendometriosisInadditiontotargetingPRDX6,furtherresearchisneededtoidentifyotherpotentialmoleculartargetsforthetreatmentofendometriosis.Dysregulationofseveralsignalingpathways,includingthePI3K/Akt/mTOR,MAPK,andWntpathways,hasbeenimplicatedinendometriosispathogenesis.Inhibitionofthesepathwayscouldpotentiallysuppressendometrioticlesiongrowthandreducepainassociatedwiththedisease.

Furthermore,endometriosisisassociatedwithchronicinflammation,andimmunecellssuchasmacrophagesandTcellsplayanimportantroleinpromotingthegrowthandsurvivalofendometrioticlesions.Strategiesthataimtomodulatetheimmuneresponseandreduceinflammationmaybeeffectiveinthetreatmentofendometriosis.

Finally,currenttreatmentsforendometriosis,suchashormonaltherapiesandsurgery,oftenhavesignificantsideeffectsandarenotalwayseffectiveinmanagingsymptoms.Developmentofnew,targetedtherapiesforendometriosisthatarelessinvasiveandhavefewersideeffectsisneeded.

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