高糖对肾脏细胞因子分泌的影响及缬沙坦的干预作用研究.docx

该【高糖对肾脏细胞因子分泌的影响及缬沙坦的干预作用研究 】是由【niuwk】上传分享，文档一共【4】页，该文档可以免费在线阅读，需要了解更多关于【高糖对肾脏细胞因子分泌的影响及缬沙坦的干预作用研究 】的内容，可以使用淘豆网的站内搜索功能，选择自己适合的文档，以下文字是截取该文章内的部分文字，如需要获得完整电子版，请下载此文档到您的设备，方便您编辑和打印。高糖对肾脏细胞因子分泌的影响及缬沙坦的干预作用研究AbstractHyperglycemiacanleadtothesecretionofvariouscytokinesinrenalcells,-2wasculturedindifferentglucoseconcentrations,andthelevelsofinterleukin-6(IL-6),tumornecrosisfactor-alpha(TNF-α),andtransforminggrowthfactorbeta-1(TGF-β1),-6,TNF-α,andTGF-β1inHK-2cellsinadose--6,TNF-α,andTGF-β1inHK-,,(DN)plicationsofdiabetes,whichcanleadtoend-stagerenaldisease(ESRD).plex,involvingmultiplefactorssuchasinflammation,oxidativestress,andadvancedglycationendproducts(AGEs)(1,2).SeveralstudieshaveshownthatinflammationplaysacrucialroleinthedevelopmentandprogressionofDN(3).Cytokinesareimportantmediatorsofinflammation,whichcancauseglomerularandtubulointerstitialinjury(4).Therefore,-1(TGF-β1)hatregulatescellproliferation,differentiation,-β1isalsoinvolvedinthepathogenesisofDNbypromotingrenalfibrosisandextracellularmatrix(ECM)accumulation(5).Interleukin-6(IL-6)hatcanstimulatetheproductionofacute-phaseproteins,promoteangiogenesis,andactivateimmunecells(6).Tumornecrosisfactor-alpha(TNF-α)hatplaysasignificantroleinthedevelopmentofDNbyinducingoxidativestress,inflammation,andapoptosis(7).ValsartanisanangiotensinIIreceptorblocker(ARB)thathasbeenshowntohaverenoprotectiveeffectsinpatientswithDN(8).Valsartancanreducebloodpressure,inhibittherenin-angiotensin-aldosteronesystem(RAAS),anddecreasethesecretionofcytokines,leadingtoareductioninrenaldamage(9).However,themechanismofvalsartan',-2wasobtainedfromtheAmericanTypeCultureCollection(Manassas,VA,USA).HK-o'sModifiedEagleMedium(DMEM)containing10%fetalbovineserum(FBS)and1%penicillin-streptomycininahumidifiedincubatorat37°Cwith5%-2cellswereseededin24-wellplatesatadensityof5×104cells/,theculturemediumwasreplacedwithDMEMcontainingdifferentglucoseconcentrations(,11,22,and44mM).After48hofincubation,,HK-2cellswereculturedinhigh-glucose(22mM)DMEMwithorwithoutvalsartan(1μM),andthelevelsofIL-6,TNF-α,andTGF-β1weremeasuredusingenzyme-linkedimmunosorbentassay(ELISA).CytokinemeasurementThelevelsofIL-6,TNF-α,andTGF-mercialELISAkits(R&DSystems,Minneapolis,MN,USA)accordingtothemanufacturer'(Bio-Rad,Hercules,CA,USA).StatisticalanalysisAlldataarepresentedasmean±standarddeviation(SD).Statisticalanalysiswasperformedusingone-wayanalysisofvariance(ANOVA)followedbyTukey'spost-<-2cellsToinvestigatetheeffectofhighglucoseoncytokinesecretioninrenalcells,HK--6,TNF-α,andTGF-β1inHK-2cellsinadose-dependentmanner(Figure1).ThelevelsofIL-6,TNF-α,andTGF-(P<).InterventioneffectofvalsartanoncytokinesecretioninHK-2cellsToinvestigatetheinterventioneffectofvalsartanoncytokinesecretioninHK-2cells,cellswereculturedinhigh--6,TNF-α,andTGF-β1inHK-2cells(Figure2).ThelevelsofIL-6,TNF-α,andTGF-β1weresignificantlylowerincellstreatedwithvalsartanthanincellswithoutvalsartan(P<).DiscussionInthisstudy,-6,TNF-α,andTGF-β1inHK-2cellsinadose--6,TNF-α,andTGF-β1inHK-,-hatcaninduceapoptosis,promoteangiogenesis,andactivateimmunecells(6).TNF-hatplaysasignificantroleinthedevelopmentofDNbyinducingoxidativestress,inflammation,andapoptosis(7).TGF-umulation,leadingtorenaldamage(5).OurresultsshowedthathighglucoseincreasedthesecretionofIL-6,TNF-α,andTGF-β1inHK-2cellsinadose-(10,11).ValsartanisanARBthathasbeenshowntohaverenoprotectiveeffectsinpatientswithDN(8).Valsartancanreducebloodpressure,inhibittheRAAS,anddecreasethesecretionofcytokines,leadingtoareductioninrenaldamage(9).OurfindingsshowedthatvalsartaninterventioncouldsignificantlyreducethesecretionofIL-6,TNF-α,andTGF-β1inHK-(12,13).Inconclusion,ourstudydemonstratedthathighglucoseincreasedthesecretionofIL-6,TNF-α,andTGF-β1inHK-2cells,,'---6,TNF-α,andTGF-±SD(n=3).*P<;#P<--2cellswereculturedinhigh--6,TNF-α,andTGF-±SD(n=3).*P<(withoutvalsartan).