简介：ObjectivesToinvestigatetheprotectiveeffectofthrombopoietin(TPO)onmyocardialcellsinvitro.MethodsH9C2celllinewasmaintainedinIscove’smodifiedDulbecco’smedium(IMDM)supplementedwith10%calfserum.Beatingcellsfromheartventriclesofneonatalheartwereculturedataninvitrosystem.Apoptosisofthecelllineabovewasinducedbytreatmentofdoxorubicin(DOX)andwasblockedbyTPO.CellsurvivalrateofH9C2cellwasmeasuredbytheMTTassay.Changesofbeatingrateofneonatalmyocardialcellswerecapturedbydigitalcameraandbeatingratewascalculated.Flowcytometrywasemployedtostudyanti-apoptoticeffectofTPObystainingJC-1proteintoH9C2cell.ResultsMTTassaydemonstratedthatdoxorubicinreducedcellsurvivalrateby73.8%±1.1%,50ng·mL-1and100ng·mL-1TPOincreasedcellsurvivalrateby84.6%±3.6%(P<0.05),86%±4%(P<0.01)atadose-dependentmanner.Beatingrateofprimaryneonatalmyocardialcellsalsodecreasedto15%±8%at48h,100ng·mL-1TPOimprovedbeatingrateto48%±11%(P<0.01).TPOdecreasedapoptoticratefrom19%±9%to11%±6%(P<0.05).ConclusionsTPOhasprotectiveeffectonmyocardialcellsinvitro.Anti-apoptosisisoneofthemechanismsbywhichTPOprotectsinjuredheart.

简介：Propofolcaninhibittheinflammatoryresponseandreducethesecretionandharmfuleffectsofastrocyte-derivedproinflammatorycytokines.Inthisstudy,afterpropofolwasinjectedintotheinjuredsciaticnerveofmice,nuclearfactorkappaBexpressionintheL4-6segmentsofthespinalcordintheinjuredsidewasreduced,apoptosiswasdecreased,nervemyelindefectswerealleviated,andthenerveconductionblockwaslessened.Theexperimentalfindingsindicatethatpropofolinhibitstheinflammatoryandimmuneresponses,decreasestheexpressionofnuclearfactorkappaB,andreducesapoptosis.Theseeffectsofpropofolpromoteregenerationfollowingsciaticnerveinjury.

简介：AbstractSevere fever with thrombocytopenia syndrome (SFTS), caused by a novel identified bunyavirus SFTS virus (SFTSV), was an emerging viral infectious disease that was firstly reported in China. There are no licensed vaccines and therapeutics against SFTSV currently. B-Propiolactone (BPL) inactivated whole virions of SFTSV strain AH12 were prepared as experimental vaccine in different antigen dose with or without Al(OH)3 adjuvant. The experimental SFTS vaccine was a satisfying immunogen, which could efficiently trigger the development of high levels of SFTSV NP-specific IgG antibodies and neutralizing antibodies against SFTSV Strain HB29 in BALB/c and C57/BL6 mice, and could induce SFTS virus-specific cellular immune responses to a certain extent. A single dose of vaccine was immunogenically insufficient in BALB/c mice; the second and third dose resulted in significant boost in antibody response. The use of Al(OH)3 adjuvant resulted in higher antibody titers. The mediate-dose of vaccine could induce as high and equivalent level of antibody titer as that of high-dose. The experimental SFTS vaccine in mediate-and high antigen dose with adjuvant resulted in solid protection of C57/BL6 mice against wild-type SFTSV challenge with markedly accelerated virus clearance from blood and spleen compared with controls. The experimental SFTS vaccine prepared in this study could efficiently elicit virus specific humoral and cellular immune responses in both BALB/c and C57/BL6 mice, and could protect C57/BL6 mice against SFTS virus challenge. These results supplied evidence that inactivated vaccine was a promising vaccine candidate for the prevention of SFTSV infection.

简介：ObjectiveToinvestigatetheprotectiveeffectsofsoundconditioningagainstsubsequenthigh-levelnoisetraumainrats.MethodRatswereexposedtoa4kHzoctavebandnoiseat95dBSPLfor10hours,thentoatraumaticexposuredose(105dBSPLfor13hours)delivered12hlater.Controlanimalswereexposuredtothetraumaticdoseonly.ABRthresholdswereobtainedbeforeandafternoiseexposure.ResultAnimalsthathadbeensoundconditioneddemonstratedlessABRthresholdshiftcomparedtothosethathadnot.ConclusionModeratelevelsoundexposureappearstohaveatougheningeffectontheratcochlea(or'conditioning')leadingtodecreasedhearinglossfromsubsequenttraumaticexposure.

简介：BACKGROUND:Ithasbeensuggestedthatmelatonin(MT)canprotectsecondaryneuronalinjury.However,theprotectiveeffectofMTonneuronalinjuryinischemia/reperfusionmodelsinvitrostillhasnotbeenproved.OBJECTIVE:ToinvestigatetheprotectiveeffectofMToncentralischemicinjuryofnervecellsandanalyzeitspossiblemechanism.DESIGN:Contrastobservationalstudy.SETTING:DepartmentofBiochemistryandMolecularBiology,TongjiMedicalCollege,HuazhongUniversityofScienceandTechnology.MATERIALS:Ratsaged7-8daysandweighing10-12gwereprovidedbyMedicalExperimentalAnimalCenter,TongjiMedicalCollege,HuazhongUniversityofScienceandTechnology,MTwasprovidedbySigmaCompany,USA.METHODS:TheexperimentwascarriedoutintheLaboratoryofBiochemistryandMolecularBiology,TongjiHospital,HuazhongUniversityofScienceandTechnologyfromOctober2002toMarch2004.TheeffectsofMTontheneurodegenerationinducedbyoxygen-glucose-deprivation(OGD)weretestedinculturedratcerebellargranulecells.NeurondamagewasquantitativelyassessedbyTypanBlueexclusionandMTTassayatdifferenttimepointsafteroxygen-glucose-deprivation(90minutes).DNAgelelectrophoresisandacridineorangestainwereperformedtodeterminethenatureofcelldamage.Andfluorescencespectrophotometerwasusedforquantificationofintracellularmalondialdehyde(MDA)atvarioustimeintervals.MAINOUTCOMEMEASURES:Correlationbetweendegreesofneuronalinjuryandreperfusiontimes,apoptosis,andproductionofMDAincells.RESULTS:①Theneuroninjurywasaggravatedwithreperfusiontime.②TheprotectiveeffectofMTwastime-anddose-dependentwhenitsconcentrationwasnothigherthan10μmol/L.⑧WhenneuronswereexposedtoOGDfor90minutes.partofthecellsexhibitedtypicalfeaturesofapoptosis:internucleosomalDNAcondensationandDNAladderonagarosegelelectrophoresis.MTaddedtocellsrecoveringfromOGDexertedneuroprotectiveactionagainstOGD-inducedapoptosis.④InOGDexposedculture

简介：Objective:Tostudytheclinicaltherapeuticeffectofanisodamineonrespiratoryfunctionafterseverebraininjury.Methods:Ninetypatientswithrespiratorydysfunctionfollowingseverebraininjuryweredividedintotwogroups:atreatmentgroup(n=45,treatedwithroutinetherapyplusanisodamine)andacontrolgroup(n=45,treatedwithroutinetherapyonly).Thepulmonaryventilationfunctionandoxygenationfunctionwerecomparedbetweenthetwogroups.Results:Inthetreatmentgroup,12hoursaftertreatmenttherespiratoryratereduced,thepartialpressureofcarbondioxide(PCO2),thepartialpressureofoxygeninarterialblood(PaO2)andoxygenationexponentincreased,thedeadspaceventilationdoseandthepulmonaryalveolus-partialpressureofarterialoxygendifferencedecreased,andtheventilationfunctionoftherespiratorytractandpulmonaryoxygenationfunctionimproved.Therewasasignificantdifferencebetweenthetwogroups(P<0.01).Noside-effectwasfoundexceptaslightincreaseofintracranialpressureandheartrate.Conclusions:Anisodaminecanimprovepulmonaryventilationfunctionandoxygenationfunctionanddecreasetheincidenceofhypoxemiamarkedly.Itiseffectiveintreatingrespiratorydysfunctionafterseverebraininjury.

简介：这研究的目的是决定包括伪-ketoacids(伪-ketoglutarate和pyruvate)，抗氧化剂的效果喂奶并且glutamate/malate联合，对老鼠精子上的氧化应力。我们的结果显示出那H2O2(250渭molL?1)导致的损坏例如损害活动性，腺苷triphosphate(ATP)弄空，精子蛋白质phosphorylation的抑制，减少的acrosome反应和减少的生存能力，能被精子的孵化显著地与伪-ketoglutarate阻止(4mmolL?1)或pyruvate(4mmolL?1)。没有在媒介的外长的H2O2，pyruvate的增加(4mmolL?1)显著地增加了superoxide阴离子(O2?在精子暂停的路)水平(P鈮?0.01)，而伪-ketoglutarate的增加(4mmolL?1)并且喂奶(4mmolL?1)有95kDa的尺寸的显著地提高的tyrosine-phosphorylated蛋白质(P鈮?0.04)。同时，伪-ketoglutarate，pyruvate，喂奶，在媒介补充的glutamate和malate能为精子活动性被用作重要精力来源和供应ATP。在结论，现在的结果证明伪-ketoacids能是为保护老鼠精子免受H2O2攻击的伤害的有效抗氧化剂并且能是有效部件改进Biggers，Whitten和Whittingham媒介的抗氧化剂能力。

简介：Theaimofthisstudyistoexpressthereceptor-bindingdomainofBacillusanthracisprotectiveantigeninE.coli.SignalsequenceoftheoutermembraneproteinA(OmpA)ofE.coliwasattachedtothe5'endofthegeneencodingprotectiveantigenreceptor-bindingdomain(the4^thdomainofPA,PALM).TheplasmidcarryingthefusiongenewasthentransformedintoE.coliandinducedtoexpressrecombinantPAlMbyIFFG.TherecombinantproteinwaspurifiedbychromatographyandthenidentifiedbyN-terrainalsequencingandWesternblot.Therecombinantprotein,about10%ofthetotalbacterialproteininvolume,wassecretedtotheperiplasmicspaceofthecell.Afterapurificationprocedureincludingionexchangechromatographyandgelfiltration,about10mgofhomogenousrecombinantPAD4wasobtainedfrom1Lculture.DatafromN-terminalsequencingsuggestedthattheaminoacidsequenceofrecombinantPAD4wasidenticalwithitsnaturalcounterpart.AndtheresultofWesternblotshowedtherecombinantproteincouldbindwithanti-PAserumfromrabbit.HighlevelsecretedexpressionofPAD4wasobtainedinE.coli.TheresultsreportedherearepartsofacontinuingresearchtoevaluatePAD4asapotentialdrugforanthraxtherapyoracandidateofnewvaccine.

简介：Propofolpreconditioninghasbeenshowntoprovideneuroprotectionagainstspinalischemia/reperfusioninjury.Inthisstudy,spinalcordischemia/reperfusioninjurywasinducedbyblockingtheabdominalaortainrabbitsfor40minutes.Resultsshowedthattheco-applicationofpropofolpreconditioningandpostconditioningregimenamelioratedpathologicalinjuryoftheischemicspinalcordandsuppressedtheelevationofmalondialdehydelevelsandincreasedsuperoxidedismutaseactivitiesinthespinalcordtissues.Co-applicationofpropofolpreconditioningandpostconditioningresultedinpotentprotectiveeffectsagainstspinalcordischemia/reperfusioninjuryandprolongedthespinalcord'stolerancetoischemia.Thisprotectionwasassociatedwiththeanti-lipidperoxidationcapacityofthespinalcordtissues.

简介：ObjectivesToinvestigatetheeffectoftelmisartanonhumanumbilicalveinendothelialcells(HUVEC)exposedtohighglucoseinvitroandtherelatedmechanism.MethodsHUVECswereincubatedwithtelmisartanandglucose(5mmol/L,30mmol/L)at0h,12h,24h,36h,48h,respectively.Thelevelofmalondialdehyde(MDA)andsuperoxidedismutase(SOD)inthesupernatantofculturedendothelialcellswasmeasuredbythiobarbituricacidtestandxanthineoxidasetest.TheexpressionofPPAR-γwasdeterminedat24hourwithWesternblottechnique.ResultsWhentheendothelialcellswereculturedinhighglucoseenvironment,theMDAlevelwassignificantlyincreased,buttheSODactivityandtheproteinexpressionofPPAR-γweremarkedlydecreased.However,thehighglucose-inducedeffectswereinhibitedbytelmisartanintervention.ConclusionTelmisartancandecreaseoxidativestressandincreasePPAR-γexpressionofendothelialcellsinhighglucoseenvironment.

简介：BackgroundRecentresearcheshavefoundthatstainscanimproveacutemyocardialischemiareperfusioninjurywhichisachievedbyinhibitinginflammatoryreaction.Xuezhikangisextractedfromredrice,atailor-madeChinesecrudedrug.MaincomponentofXuezhikangthatcaninhibitblood-fatisstatins.MethodsFortyhealthySDrats(halfmaleandhalffemale,200gorso)wererandomlydividedintofourgroups:A:normalcontrol;B:shamoperation;C:MIRgroup;D:Xuezhikanggroup.Theacutemyocardialischemiareperfusioninjurymodelwasproduced.Infarctsizes,MYO,CK-MB,cTnI,IL-10andIL-18weredetectedafterreperfusion.ResultsComparedwithCandDgroup,inAandBgroup,infarctsizewereincreasedsignificantly(P<0.01),thelevelofserumMYO,CK-MB,cTnIwereincreasedsignificantly(P<0.01),thelevelofIL-10weredecreasedsignificantly(P<0.01)andIL-18,CRPwereincreasedsignificantly(P<0.01).ComparedwithCgroup,infarctsizeweredecreasedsignificantly(P<0.05),thelevelofserumMYO,CK-MBandcTnIwereincreasedsignificantly(P<0.05),thelevelofIL-10wereincreasedsignificantly(P<0.05)andIL-18weredecreasedsignificantly(P<0.05).ThelevelofIL-10andIL-18werenodifferencebetweenAandBgroup.ConclusionTheapplicationofXuezhikangcapsulesonratsbeforetheoperationofmyocardialischemiareperfusioncanlesseninflammatoryreactionandreduceinfarctsizesandprotectacutemyocardialischemiareperfusion.

简介：ShouwuisatraditionalChinesemedicine(TCM)withneuroprotectiveeffect.ShouwuYizhidecoction(SYD)wasdesignedbasedonTCMtheory.However,littleisknownabouttherolesofSYDinVasculardementia(VaD).ThepresentstudyaimedtoevaluatethepotentialeffectsofSYDonthevascularcognitiveimpairmentandexploretheunderlyingmechanismbyestablishingfocalcerebralischemia/reperfusion(I/R)ratmodeltoinduceVaD.SYDadministration(54mg·kg~(-1))for40daysobviouslyimprovedthevascularcognitiveimpairmentinthemiddlecerebralarteryocclusion(MCAO)ratsasevidencedbythedeclinedneurologicaldeficitscoreandshortenedescapelatencyvianeurologicaldeficitassessmentandMorriswatermazetest.Moreover,SYDdecreasedneurondamage-inducedcelldeathandamelioratedtheultrastructureofendothelialcellsintheMCAOrats,therebyalleviatingVaD.Mechanistically,SYDcausedincreasesintheexpressionofvascularendothelialgrowthfactor(VEGF),CD34andCD31,comparedwiththeMCAOratsincoronalhippocampus.Simultaneously,theexpressionlevelofmiR-210waselevatedsignificantlyafterSYDadministration,comparedwiththevehiclerats(P<0.01).TheexpressionofNotch4atbothmRNAandproteinlevelswasupregulatedremarkablyalongwiththenotablydownregulatedDLL4expressionunderSYDadministrationcomparedwiththevehiclerats(P<0.05).Overall,theaboveresultsindicatedthatSYDpromotedangiogenesisbyupregulatingVEGF-inducedmiR210expressiontoactivateNotchpathway,andfurtheralleviatedneurondamageandamelioratedtheultrastructureofendothelialcellsintheMCAOrats,ultimatelyenhancingthecognitionandmemoryofMCAOrats.Therefore,ourfindingspreliminarilyidentifiedtheeffectandthemechanismofactionforSYDonVaDinrats.SYDcouldbeapotentialcandidateintreatmentofVaD.

简介：AbstractPositive Pressure Protective Clothing (PPPC) is the most important personal protective equipment for BSL-4 laboratory and a primary barrier to avoid exposure to pathogenic microorganisms. However, during the process of storage, utilization, disinfection and inspection, it will be inevitable damaged in varying degrees. PPPC is expensive; therefore, effective repairs become an important procedure to prolong service life of PPPC and to ensure their protective function. This paper analyzed those common damages in PPPC during routine BSL-4 laboratory operations and provided repair plans which can be used as references for users and maintenance personnel.

简介：AbstractObjective:Clinically, low-dose aspirin and progesterone are frequently used to prevent pregnancy loss. We investigated the effect of these drugs on the biological behavior of human extravillous trophoblasts in vitro.Methods:HTR-8/SVneo cells were cultured in vitro and treated with different concentrations of aspirin and progesterone. The proliferation, invasion, and apoptosis of HTR-8/SVneo cells were assessed using a cell counting Kit-8 assay, Matrigel Transwell assay, and Hoechst staining, respectively. Reverse transcriptase polymerase chain reaction was used to verify the expression of related genes. Reactive oxygen species (ROS) levels were detected using the 2,7-dichlorofluorescin diacetate assay.Results:Low-dose aspirin alone, progesterone alone, or aspirin plus progesterone upregulated the proliferation and invasion and decreased the apoptosis of HTR-8/SVneo cells. Moreover, the expression of marker of proliferation Ki-67 (MKI67), matrix metalloproteinases 2 (MMP2), and MMP9 was increased. In addition, low-dose aspirin plus progesterone exerted stronger anti-apoptosis effects than low-dose aspirin and progesterone alone. Interestingly, aspirin upregulated the expression of progesterone receptor (PGR). Treatment with hydrogen peroxide (H2O2) promoted ROS production in HTR-8/SVneo cells; however, low-dose aspirin plus progesterone significantly restricted H2O2-mediated ROS production and apoptosis in HTR-8/SVneo cells.Conclusions:These data suggest that low-dose aspirin and progesterone promote proliferation and invasion and cooperatively reduce oxidative stress and apoptosis in trophoblasts in vitro. These results may provide an experimental basis for the combined application of aspirin and progesterone to prevent unexplained recurrent spontaneous miscarriage, especially in patients with trophoblast dysfunction.

简介：无

简介：目的methotrexate(MTX)的最重要的副作用是mucositis。这研究的目的是在收到methotrexate的老鼠在肠的损坏和氧化应力上评估沉金摘录的效果。方法实验在划分成六个组的男Wistar白化体老鼠上被执行。首先组织收到的正常盐口头上地，第二个组收到了沉金摘录(100mg瑡潩?????????????????假吗？？

简介：瞄准：调查17β-estradiol(E2)的效果，Peganum伤害翼摘录(PHE)和各种各样的睾丸参数上的热量的限制(CR)在老化期间。方法：Twelve-month-old雄的老鼠与E2或PHE被对待6个月，或提交了到CR(40%)。结果：我们的结果证明雌激素和CR能由象aromatase和雌激素受体基因表情的减少一样阻止睾丸激素和E2层次的减少保护男性腺。确实，E2，PHE和CR处理在超级氧化物dismutase活动导致了增加并且减少阴囊的酶的活动：gamma-glutamyltransferase，碱的磷酸酶，喂奶deshydrogenase以及aspartate并且喂奶在年老的动物的transaminases。另外，阴囊的过氧化氢酶和gluthationeperoxidase活动在18月年龄与未经治疗的动物相比在E2，PHE和对待CR的老鼠被提高。而且，estradiol，PHE和CR的积极效果被类脂化合物的底层进一步每氧化支持。精子发生的恢复在对待的老鼠被记录。结论：除为精子发生有益的一本低热量的食谱以外，雌激素的一个保护的antioxydant角色被建议。雌激素推迟阴囊的房间损坏，它导致功能的老朽并且，因此雌激素在保护繁殖功能免受在年老的睾丸在大数量生产的反应的氧种类(ROS)施加的不利效果的伤害是有用的。

简介：

简介：瞄准：在成年老鼠的睾丸由FA对氧化损坏在睾丸和维生素Ｅ(VE)的保护的效果上调查甲醛(FA)的效果。方法：三十只老鼠随机被划分成三个组：(1)控制；(2)FA处理组织(脂肪)；并且(3)胖+VE组织。胖、胖的+VE组被吸入在10mg/m(3)的集中暴露于FA2个星期。另外，胖+VE组在2星期的FA处理期间是口头上地管理的VE。在精子的处理，在睾丸的组织病理学说、生物化学的变化，以及数量和质量以后，被观察。结果：精子的阴囊的重量，数量和质量，超级氧化物歧化酶(草皮)的活动，而malondialdehyde(MDA)的水平显著地在控制组与那些相比在胖组在老鼠的睾丸被增加，谷胱甘肽过氧化物酶(GSH-Px)和谷胱甘肽(GSH)显著地被减少。VE处理在胖+VE组恢复了这些参数。另外，有hematoxylin曙红的显微镜学(他)染色证明细精管萎缩的、生精的上皮细胞瓦解了，在在胖组和VE处理的老鼠的shed显著地在胖+VE改进了阴囊的结构组。结论：在由导致氧化应力的成年老鼠的阴囊的结构和功能，和这损坏能部分是的FA破坏由VE逆行。

简介：Inthepresentstudy,theinvolvementofL-arginine(L-Arg)NOoniheprotectiveactionofelectroacupuncture(EA)oncerebralischemicinjurywasobservedinacuteischemia-reperfusion(IR)ratmodelbytakingregionalcerebralbloodflow(r-CBF),cerebralwatercontent(CWC),andbloodnitricoxide(NO)contentsasindexes.Resultsshowedthat1)EAcouldcauser-CBFandserumNOcontenttoincreaseandCWCtolower,suggestinganprotectiveactionofEAonIRcerebralinjury;2)intravenousinjectionofL-ArgalsohadanprotectiveeffectoncerebralIRcerebralinjury,whileL-NNAhadnothiseffect;and3)pre-treatmentwithL-ArgmightstrengthentheeffectofEAfurther,whilepretreatmentwithL-NNAcouldweakenitseffect.ItindicatesthatL-Arg-NOmaybeinvolvedintheeffectofEAinprotectingthebrainfromischemicinjury.