简介：AIMTo在透镜调查Aquaporin-1(AQP-1)的角色上皮的房间(LEC)和它的潜在的目标基因。AQP-1明确地在眼睛的LEC被表示并且为透镜动态平衡和透明性维护是重要的。此处，在LEC的AQP-1表示被调查在奔流formation.METHODSLECs与它的潜在的角色联合在房间幸存上评估它的影响是有带AQP-1的lentivirus的transfected小介入RNA(siRNA)。实时聚合酶链反应(PCR)并且西方的弄污被进行从不同的组在LEC检测AQP-1表示。同时，房间数kit-8(CCK-8)试金和流动cytometry被执行测量LEC增长和apoptosis，respectively.RESULTSAQP-1表示显著地在LEC被减少，两个都在mRNA和蛋白质铺平(P<；0.05)，在siRNA处理以后。减少的房间生存能力被CCK-8试金与siRNA干扰在LEC检测，与控制房间相比(P<；0.05)。apoptosis率显著地在siRNA干扰以后在房间增加了(P<；0.05).CONCLUSIONThe减少了在规定下面的房间生存能力追随者AQP-1大部分由于它LEC的apoptosis的正式就职。AQP-1减小可能在LEC导致生理的功能的变化，它可能与奔流的出现和发展被联系。

简介：GinsenosideRg1（Rg1）hasanti-agingandanti-neurodegenerativeeffects.However,themechanismsunderlyingtheseactionsremainunclear.TheaimofthepresentstudywastodeterminewhetherRg1affectshippocampalsurvivalandneuriteoutgrowthinvitroafterexposuretoamyloid-betapeptidefragment25–35(Aβ25–35),andtoexplorewhethertheextracellularsignal-regulatedkinase（ERK）andAktsignalingpathwaysareinvolvedinthesebiologicalprocesses.Weculturedhippocampalneuronsfromnewbornratsfor24hours,thenaddedRg1tothemediumforanother24hours,withorwithoutpharmacologicalinhibitorsofthemitogen-activatedproteinkinase（MAPK）familyorAktsignalingpathwaysforafurther24hours.Wethenimmunostainedtheneuronsforgrowthassociatedprotein-43,andmeasuredneuritelength.Inaseparateexperiment,weexposedculturedhippocampalneuronstoAβ25–35for30minutes,beforeaddingRg1for48hours,withorwithoutAktorMAPKinhibitors,andassessedneuronalsurvivalusingHoechst33258staining,andphosphorylationofERK1/2andAktbywesternblotanalysis.Rg1inducedneuriteoutgrowth,andthiseffectwasblockedbyAPI-2（Aktinhibitor）andPD98059（MAPK/ERKkinaseinhibitor）,butnotbySP600125orSB203580（inhibitorsofc-JunN-terminalkinaseandp38MAPK,respectively）.Consistentwiththiseffect,Rg1upregulatedthephosphorylationofAktandERK1/2;theseeffectswerereversedbyAPI-2andPD98059,respectively.Inaddition,Rg1significantlyreversedAβ25–35-inducedapoptosis;thiseffectwasblockedbyAPI-2andPD98059,butnotbySP600125orSB203580.Finally,Rg1significantlyreversedtheAβ25–35-induceddecreaseinAktandERK1/2phosphorylation,butAPI-2preventedthisreversal.OurresultsindicatethatRg1enhancesneuriteoutgrowthandprotectsagainstAβ25–35-induceddamage,andthatitsmechanismmayinvolvetheactivationofAktandERK1/2signaling.更多还原

简介：Manystudiesdemonstratethatconventionalanticancerdrugselevateintracellularlevelofreactiveoxygenspecies(ROS)andalterredox-homeostasisofcancercells.ItiswidelyacceptedthatanticancereffectofthesechemotherapeuticsisduetoinductionofoxidativestressandROS-mediatedapoptosisincancer.Ontheotherhand,theharmfulsideeffectsofconventionalanticancerchemotherapyarealsoduetoincreasedproductionofROSanddisruptionofredox-homeostasisofnormalcellsandtissues.ThisarticledescribesthemechanismsfortriggeringandmodulationofapoptosisthroughROS-dependentandROS-independentpathways.Wetrytoanswerthequestion:'Isitpossibletoinducehighlyspecificapoptosisonlyincancercells,withoutoverproductionofROS,aswellaswithoutharmfuleffectsonnormalcellsandtissues?'Thereviewalsosuggestsanewtherapeuticstrategyforselectivekillingofcancercells,withoutsignificantimpactonviabilityofnormalcellsandtissues,bycombininganticancerdrugswithredox-modulators,affectingspecificsignalingpathwaysandavoidingoxidativestress.

简介：Marsdeniaetenacissimaeextract(MTE),commonlyknownasXiao-Ai-PinginChina,isatraditionalChineseherbmedicinecapableofinhibitingproliferationandmetastasisandboostingapoptosisinvariouscancercells.However,littleisknownaboutthecontributionofMTEtowardstumorangiogenesisandtheunderlyingmechanism.ThepresentstudyaimedtoevaluatetheeffectsofMTEontheproliferationandapoptosisofhumanumbilicalveinendothelialcells(HUVECs)andthemolecularism.3-(4,5-dimethylthiazol-2-yl)-5(3-carboxymethoxyphenyl)-2-(4-sulfopheny)-2H-tetrazolium,innersalt(MTS)andPI-stainedflowcytometryassaysrevealedthatMTEdose-dependentlyreducedtheproliferationofHUVECsbyarrestingcellcycleatSphase(P<0.05).AnnexinV-FITC/PI-stainedflowcytometryconfirmedthatMTE(160μL·mL-1)enhancedtheapoptosisofHUVECssignificantly(P<0.001).Real-timequantitativeRT-PCRandWesternblotanalysesshowedanincreaseinBaxexpressionandasharplydeclineinBcl-2expression;caspase-3wasactivatedsimultaneouslyinadose-dependentmanner(P<0.05).Furtherstudyobservedthedose-dependentdown-regulationofvascularendothelialgrowthfactor(VEGF)receptor-2(VEGFR-2),P2Y6receptor(P2Y6R),andchemokine(C-Cmotif)ligand2(CCL-2),alongwiththeactivationofPKCδandup-regulationofp53inadose-dependentmannerinMTE-treatedselectedcells(P<0.05).Collectively,theresultsfromthepresentstudysuggestedthatMTEsuppressedtheproliferationbyattenuatingCCL-2-mediatedVEGF/VEGFR2interactionsandpromotedtheapoptosisthroughPKCδ-inducedp53-dependentmitochondrialpathwayinHUVECs,supportingthatMTEmaybedevelopedasapotentanti-cancermedicine.