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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

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简介：在细胞的增长和内长的脉管的endothelial生长因素(VEGF)上调查melatonin的效果的目的在胰腺的癌房间(PANC-1)的表示。方法PANC-1房间为这研究是有教养的。在文化媒介的分泌VEGF集中用ELISA方法被决定，在肿瘤房间的VEGF生产被immunocytochemistry，和VEGFmRNA表示检测被RT-PCR决定。更高结果melatonin集中显著地禁止了细胞的增长，与展出最高禁止的效果的1mmol/L集中(P<0.01)。在房间文化上层清液和intra小房的VEGF集中都显著地在melatonin(1mmol/L)以后被减少孵化(P<0.05)。VEGFmRNA表示在观察时期期间以一种时间依赖者方式显著地减少了(P<0.05)。结论高melatonin集中显著地禁止了胰腺的癌房间的增长。内长的VEGF表示被melatonin孵化也压制。

简介：目的：研究针刺降压和褪黑素（Mel）在下丘脑前核（AHA）引起应激性高血压大鼠血压降低的作用是否与延髓头端腹外侧区（rVLM）氨基酸类递质释放的改变有关，并分析Mel降压机制与针刺降压机制之间的关系。方法：采用足底电击结合噪声的方法建立应激性高血压大鼠模型：针刺应用电针的方法，穴位取双侧足三里：采用中枢核团微量注射的方法给药，观察动脉血压的改变，同时应用脑内微透析的方法取样，并利用高效液相色谱．荧光检测的方法，分析透析液中氨基酸含量的改变。结果：大鼠在接受应激处理后，血压升高，rVLM内谷氨酸（Glu）释放量增加，应激性高血压大鼠在经针刺处理后，血压回降，rVLM内Glu释放量回减。微量注射Mel至应激性高血压大鼠的AHA能使血压降低，rVLM内Glu释放量也减少，而γ-氨基丁酸（GABA）和牛磺酸（Tau）释放量则增加。在rVLM微量注射GABA。受体拮抗剂荷包牡丹碱（bicuc）则可部分阻断Mel在AHA引起的降压效应。结论：针刺降压与rVLM内Glu释放量减少有关，而Mel在AHA引起的降压效应则与rVLM内Glu释放量减少，以及GABA和Tau释放量增加有关。针刺降压和Mel在AHA引起的降压机制都与rVLM内Glu释放量减少有关。

简介：瞄准：为了在streptozotocin(STZ)的阴囊的组织每氧化(LPO)和抗氧化剂酶的活动在类脂化合物上检验melatonin治疗的效果，导致了糖尿病的老鼠。方法：26只雄的老鼠随机如下被划分成三个组：组我，控制，非糖尿病的老鼠(n=9)；组II，导致STZ的、未经治疗的糖尿病的老鼠(n=8)；组III，导致STZ，对待melatonin(10mg/kg的剂量。白天)糖尿病的老鼠(n=9)。后面的8星期的melatonin处理，所有老鼠被使麻木然后被打死把睾丸从阴囊移开。结果：作为与组相比我，在老鼠组II的阴囊的纸巾，malondialdehyde(MDA)的增加的层次(P<0.01)并且超级氧化物歧化酶(草皮)(P<0.01)象过氧化氢酶(猫)的减少的层次一样(P<0.01)并且谷胱甘肽过氧化物酶(GSH-Px)(P>0.05)被发现。相反作为与组II相比，在老鼠组III的阴囊的纸巾，MDA的层次减少了(但是这减少不是重要的，P>0.05)并且草皮(P<0.01)象猫一样(P<0.05)增加。GSH-Px没被任何处理影响。Melatonin显著地没影响糖尿病的组的提高的葡萄糖集中。在学习的结束，借助于身体和阴囊的重量在对待melatonin的组和未经治疗的组之间没有有效差量。结论：糖尿病增加氧化应力，melatonin每氧化和力量禁止类脂化合物调整糖尿病的老鼠睾丸的抗氧化剂酶的活动。

简介：Freeradicalsinducedbytraumaticbraininjuryhavedeleteriouseffectsonthefunctionandantioxidantvitaminlevelsofseveralorgansystemsincludingthebrain.Melatoninpossessesantioxidanteffectonthebrainbymaintainingantioxidantenzymeandvitaminlevels.Weinvestigatedtheeffectsofmelatoninonantioxidantabilityinthecerebralcortexandbloodoftraumaticbraininjuryrats.Resultsshowedthatthecerebralcortexβ-carotene,vitaminC,vitaminE,reducedglutathione,anderythrocytereducedglutathionelevels,andplasmavitaminClevelweredecreasedbytraumaticbraininjurywhereastheywereincreasedfollowingmelatonintreatment.Inconclusion,melatoninseemstohaveprotectiveeffectsontraumaticbraininjury-inducedcerebralcortexandbloodtoxicitybyinhibitingfreeradicalformationandsupportingantioxidantvitaminredoxsystem.

简介：Inthisstudy,wesoughttoelucidatetheeffectsofmelatoninonlearningandmemoryaswellasapoptosisandexpressionoftheBaxorBcl-2proteinsinthesubgranularzoneofthedentategyrusinpinealectomizedrats.UsingtheMorriswatermazeandtheolfactorymemorytests,wefoundthattheaverageescapelatencyinpinealectomizedratswasclearlyincreasedcomparedwithsham-operatedrats.Moreover,theaverageescapelatencyinthemelatonin-treatedandpinealectomizedratswaslongerthanthatinthesham-operatedratsandshorterthanthatinthepinealectomizedanduntreatedrats.Immunohistochemistryandterminal-deoxynucleoitidyltransferasemediatednickendlabeling(TUNEL)showedthattherewerefewerBaximmunoreactivecellsandTUNEL-positive(apoptotic)cellsbutmoreBcl-2immunoreactivecellsinthemelatonin-treatedratscomparedwiththepinealectomizedrats.Thesham-operatedratsshowednumbersofthesecellssimilartothemelatonin-treatedrats.TheseexperimentalfindingsdemonstratethatmelatonintreatmentmayreduceabnormalapoptosisbypromotinggeneexpressionofBaxandsuppressinggeneexpressionofBcl-2inthesubgranularzoneofthedentategyrusinpinealectomizedrats.Theseeffectsappeartoresultintheinhibitionofcellularapoptosisandtheimprovementofspatiallearningandmemoryinpinealectomizedrats.

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