简介:Theactiveingredientofginseng,ginsenosidesRg1,hasbeenshowntoscavengefreeradicalsandimproveantioxidantcapacity.ThisstudyhypothesizedthatginsenosidesRg1hasaprotectiveroleinhumanneuroblastomacellsinjuredbyH_2O_2.GinsenosidesRg1atdifferentconcentrations(50and100μM)wasusedtotreatH_2O_2(150μM)-injuredSH-SY5Ycells.ResultsdemonstratedthatginsenosideRg1elevatedthesurvivalrateofSH-SY5YcellsinjuredbyH_2O_2,diminishedtheamountofleakedlactatedehydrogenase,andincreasedsuperoxidedismutaseactivity.GinsenosideRg1effectivelysuppressedcaspase-3immunoreactivity,andcontributedtoheatshockprotein70geneexpression,inadose-dependentmanner.TheseresultsindicatethatginsenosideRg1hasprotectiveeffectsonSH-SY5YcellsinjuredbyH_2O_2andthatitsmechanismofactionisassociatedwithanti-oxidationandtheinhibitionofapoptosis.
简介:目的同步考量脑损伤后大鼠与认知功能较为密切的脑区N-甲基-D-天冬氨酸受体1(NMDAR1)表达与认知功能的变化。方法参照Feeney法建立大鼠创伤性脑损伤模型,伤后1d,2d,4d,7d1).2免疫组化SABC法检测大鼠额叶皮质、海马区、基底前脑区NMDAR1表达,以行走实验、平衡实验及记忆功能测定评估大鼠认知障碍变化。结果轻、中型脑损伤组大鼠于伤后2d认知障碍最严重,分别于伤后3,7d基本恢复正常。轻型、中型脑损伤组脑额叶皮质、海马区、基底前脑区NMDAR1均于伤后1d升高,于2d降至较低水平后再呈缓慢增高趋势,与认知障碍变化趋势呈同步变化,且中型脑损伤组NMDAR1表达高于假手术组与轻型脑损伤组(P〈0.05)。结论大鼠经创伤性脑损伤后,额叶皮质、海马区、基底前脑区细胞中的NMDAR1含量和损伤后认知障碍的变化趋势有相似性;创伤性脑损伤后表达增加的NMDAR1对大鼠认知功能有加重损害作用。
简介:BACKGROUND:Animalexperimentshaveconfirmedthatbonemarrowstromalcell(BMSC)transplantationcanserveasatreatmentforepilepsy.OBJECTIVE:BMSCsderivedfromgreenfluorescentprotein(GFP)miceweretransplantedintothehippocampalCA1regionofepilepticrats.Theaimofthestudywastorecordelectroencephalogram(EEG),analyzesurvivalandmigrationofBMSCs,andvalidatetheeffectofBMSCtransplantationforthetreatmentofepilepsy.DESIGN,TIMEANDSETTING:ArandomizedblockdesignexperimentwasperformedattheInstituteofNeuroscience,KunmingMedicalCollegefromMarch2005toFebruary2006.MATERIALS:HomozygousC57BL/6CrSlcTgN(acr-EGFP)OsbC14-Y01-FM131mice,8-12weeksofage,wereselectedforpreparationofcellsuspension.SpragueDawleyratswereselectedforestablishingepilepsymodels.METHODS:Ratswererandomlydividedinto4groups:control(n=8),model(n=8),normalsaline(n=24),andBMSC(n=24).Inthemodel,normalsaline,andBMSCgroups,epilepsywasestablishedwithpenicillin(3×107U/kgi.p.×7days).RatsintheBMSCgroupreceivedaBMSCsuspensionderivedfromgreenfluorescentproteinmiceintotherighthippocampalCA1region.RatsinthevehiclecontrolgroupwereinjectedwiththesamevolumeofnormalsalineintothehippocampalCA1region.MAINOUTCOMEMEASURES:Theelectroencephalogramwasusedtomonitorbrainactivity.SurvivalandmigrationofthetransplantedBMSCswasobservedusingfluorescencemicroscopyat1,2,and4weeksaftertransplantation.RESULTS:InBMSCgroup,fluorescentcellswereobservedatthetransplantationsiteandintheadjacenttissue,aswellasinthetissuesurroundingtheneedletract,indicatingthemigrationofimplantedcells.Fluorescentcellswerenotdetectedinthevehiclecontrolgroup.Theelectroencephalogramofthecontrolanimalsexhibited7-9Hzαwaves,withawaveamplitude<50μV.Inthemodelandvehiclecontrolgroups,randomspike-and-wavedischargesofthesharpspike-sharplowwavetyp
简介:目的探讨Notch信号通路在人脑胶质瘤发展中的作用。方法收集脑胶质瘤组织标本60例,其中Ⅰ-Ⅱ级胶质瘤35例及Ⅲ-Ⅳ级胶质瘤25例,并取22例瘤旁正常脑组织标本作为对照。采用半定量RT-PCR方法检测这些标本中Notch-lmRNA的表达。结果Notch-1mRNA在人脑胶质瘤中的表达显著高于正常脑组织(P〈0.01),且在Ⅲ~Ⅳ级胶质瘤组中的表达显著高于Ⅰ-Ⅱ级组(P〈0.01)。相关性研究发现,Notch-1mRNA的表达与人脑胶质瘤病理分级呈正相关(r=0.706,P〈0.01)。结论Notch-1mRNA在人正常脑组织和脑胶质瘤中均有表达,但其在脑胶质瘤中的表达与脑胶质瘤的病理分级呈正相关。
简介:梅毒是我国目前主要的性传播疾病之一,国内神经梅毒发病率已高于欧美国家。梅毒若不规范治疗,将转变为神经梅毒,对神经系统造成严重损害,应引起广大医务工作者注意。文献中仅表现为复视、非阿-罗瞳孔的神经梅毒尚未见报道,现报告一例以复视为表现的不典型神经梅毒并文献复习。1病例报告1.1病史特点患者男,54岁,已婚,干部,因复视25天入院,患者25d前无诱因出现复试,无视力下降,无头痛、呕吐,无发热,无肢体活动障碍,患者双眼看物体时超过2米时复视明显,但是用一只眼睛看东西时无复视。既往体健,患者无高血压、糖尿病、高血脂及心脏病史,有冶游史10年。
简介:目的探讨实质型多形性黄色瘤型星形细胞瘤(PXA)的临床、影像学表现、病理学特点及致痫机制和外科治疗方案。方法回顾性分析1例PXA患儿的临床资料。结果患儿男,10岁,临床表现为反复癫痫发作。脑电图示右颞区为主的慢波、棘-慢波发放,头颅MRI平扫见右颞中部皮质结构异常,增强扫描局部呈不均匀片状强化。术中见病变位于右侧颞中回后部,局部皮质略肿胀、颜色稍黄、质地偏韧、边界欠清,自皮质表面向深部生长。术中皮质脑电图(ECoG)监测见癫痫放电主要位于病变及其周围皮质,扩大切除病变后再次监测未见异常癫痫波发放。术后随访9个月无癫痫发作。结论PXA是一种少见的中枢神经系统肿瘤,多以癫痫发作为首发症状。在ECoG监测下行病变扩大切除是治疗PXA的有效方法。
简介:BACKGROUND:Epidemiologicstudieshaveindicatedthattheincidenceofstrokeinpremenopausalfemalesislowerthaninmalesatthesameage,butitsignificantlyrisesinpostmenopausalfemales.Estrogenisusedclinicallytoalleviateinjurycausedbycerebralischemia.Ithasbeenhypothesizedthattheneuroprotectiveroleofestrogenrelatestoangiopoietin(Angpt),whichplaysanimportantroleinvascularization,vascularremodelingandmaturation.OBJECTIVE:Toobserveandvalidatetheeffectofestradiolonangiopoietin-1(Angpt1)mRNAexpressioninovariectomizedratswithfocalcerebralischemiaafterreperfusion,soastoexplorethemolecularmechanismsofestradiol-mediatedprotectionfromcerebralischemicdamage.DESIGN,TIMEANDSETTING:Randomized,controlled,molecularbiology,prospectiveanimalstudy.TheexperimentwasperformedattheCentralLaboratoryofChongqingMedicalUniversityfromSeptembertoDecember2005.MATERIALS:Fiftyhealthyfemalewildtype(WT)ratsaged6monthsandfiftyfemaleratsaged6monthswithknockoutoftheestrogen-alphareceptorgene(ERKO).METHODS:WTratsandERKOratsweredividedintoestradiolandcontrolgroups(n=25),andinjectedin-tramuscularlywithestradiolbenzoate(100μg/kgperday)orcornoil(1mL/kgperday)for7days,30daysafterbilateralovariectomy.Ratmodelsofcerebralischemia/reperfusionwereestablishedwiththemiddlecerebralarteryocclusionmethod.After30minutesofmiddlecerebralarteryocclusion,ratsfromtheestradiolandcontrolgroupswereinjectedintramuscularlywithestradiolbenzoateorcornoilattheabovedose.MAINOUTCOMEMEASURES:Weusedradio-immunityanalysisandlaser-Dopplerflowmetrytomeasureplasmaestradiollevelsandchangesincerebralbloodflow.WeusedimmunohistochemicalstainingofCD34epitopestomeasurechangesinthecapillarydensityinbrainfollowingcerebralischemia/reperfusion,andquantitativeRT-PCRanalysistoassessmRNAexpressionlevelsofAngpt1,Angpt2,Tie2,vascu
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简介:BACKGROUND:Drugaddictioninvolvestwomaincentralnervoussystems,namelythedopamineandnoradrenalinesystems.Thesesystemsareprimarilydistributedinfivebrainregions:theventraltegmentalarea,thenucleusaccumbens,theprefrontalcortex,thehippocampus,andthelocuscoeruleus.OBJECTIVE:Toinvestigateregionalchangesofguaninenucleotidebindingprotein-inhabitant2(Gi2)indopaminergicandnoradrenergicneuronsinbrainsofmorphine-tolerantand-dependentrats.DESIGN,TIME,ANDSETTING:ArandomizedcontrolstudywasperformedattheDepartmentofNeu-robiologyintheSecondMilitaryMedicalUniversityofChinesePLA(Shanghai,China)betweenSeptember2002andMarch2004.MATERIALS:Thirty-six,healthy,male,Sprague-Dawley(SD)ratswereusedtoestablishmorphine-dependentmodels.MorphinehydrochloridewasaproductofShenyangFirstPharmaceuticalFactory(China);naloxonehydrochloridewasaproductofBeijingFour-RingPharmaceuticalFactory(China);andαsubunitofGi2antibodywasofferedbySantaCruzBiotechnology,Inc(USA).METHODS:Thirty-sixSDratswererandomlydividedintosixgroups(n=6):(1)acutemor-phine-dependentgroup,(2)acuteabstinentgroup,(3)acutecontrolgroup,(4)chronicmorphine-dependentgroup,(5)chronicabstinentgroup,and(6)chroniccontrolgroup.Ratsintheacutemorphine-dependentandtheacutegroupswereinjectedwithmorphine(5mg/kg),oneinjectioneverytwohours,foratotalofeightinjections.Intheacuteandchronicmorphine-dependentratmodels,morphinewithdrawalsyndromewasprecipitatedbyaninjectionofnaloxone(5mg/kg).Ratsintheacutecontrolgroupweregivenaperitonealinjectionofphysiologicalsalineatthesameadministrationtimeastheabovetwogroups.Ratsinthechronicmorphine-dependentandchronicabstinentgroupswereinjectedwithmorphinethreetimesperday.Theadministrationdoseonday1wasinitially5mg/kgat20:00,whichincreasedby5mg/kgat8:00,12:00,and20:00untilday7.Onday
简介:BACKGROUND:Calciumion(Ca2+)overloadplaysanimportantroleincerebralischemia/reperfusioninjury.Anisodamine,atypeofalkaloid,canprotectthemyocardiumfromischemiaandreperfusioninjurybyinhibitingintracellularcalcium[Ca2+]ioverload.OBJECTIVE:Toinvestigateeffectsofanisodamineon[Ca2+]iconcentrationandcortexultrastructurefol-lowingacutecerebralischemia/reperfusioninrabbits.DESIGN,TIMEANDSETTING:RandomizedandcontrolledtrialwasperformedattheDepartmentofEmergency,TongjiHospital,TongjiMedicalCollegeofHuazhongUniversityofScienceandTechnologyfromSeptembertoDecember2006.MATERIALS:Fortyhealthyrabbitswereusedtoestablishmodelsofacutecerebralischemia/reperfusion.AnisodaminewasprovidedbyLianyungangDongfengPharmaceuticalFactory;Fura-2waspurchasedfromNanjingJianchengBioengineeringInstitute;dual-wavelengthfluorescentspectrophotometrysystemandDM-300softwarewereprovidedbyBio-Rad,USA;OPTON-EM10CtransmissionelectronmicroscopewasproductofSiemens,Germany.METHODS:Fortyrabbitswererandomlydividedintothefollowinggroups:shamoperation,ischemia,ischemia/reperfusion,andanisodamine,withtenrabbitsineachgroup.Modelsofcompletecerebralischemiainjurywereestablished.Inaddition,bloodwascollectedfromthefemoralarteryofratsintheischemia/reperfusionandanisodaminegroupstoinducehypotensionandestablishreperfusioninjurymodels.Thebilateralcommoncarotidarteryclampwasremovedfromtheanisodaminegroup20minutesafterischemia,andanisodamine(10mg/kgbodymass)wasinjectedviathefemoralvein.Rabbitsintheshamoperationgroupunderwentonlyvenouscannulation.MAINOUTCOMEMEASURES:[Ca2+]iconcentrationwasdeterminedusingadual-wavelengthfluorescentspectrophotometrysystem,andcorticalultrastructurewasobservedfollowinguranyl-leadcitratestaining.RESULTS:Thelevelsof[Ca2+]iintheischemiaandischemia/reperfusiongroupsweresignificantlyin-creased,c
简介:目的探讨GATA-3及Th2细胞因子IL-4与多发性肌炎(PM)/皮肌炎(DM)的关系。方法用RT-PCR方法检测PM/DM患者外周血单个核细胞(PBMC)中GATA-3、IL-4的mRAN表达,并与正常健康人进行比较。结果PM、DM组中GATA-3mRNA表达阳性率(85.7%,86.4%)均高于正常对照组(25%)(P〈0.05);PM、DM组GATA-3的表达强度(0.268,0.411)均高于正常对照组(0.000)(P〈0.05);皮肌炎IL-4mRNA的表达强度(0.251)高于正常对照组(0.000)(P〈0.05);GATA-3与IL-4的表达强度呈正相关(r=0.475,P〈0.05)。结论皮肌炎的Th2细胞过度分化及体液免疫增强可能与GATA-3表达增强有关。
简介:目的探讨褪黑素通过调节核苷酸结合寡聚化结构域样受体3炎症复合体(NLRP3)对蛛网膜下腔出血(sAH)后早期脑损伤(EBI)的保护作用和机制。方法建立小鼠颈动脉线穿法SAH模型,分为假手术组、假手术+溶剂组、SAH+溶剂组和SAH+褪黑素组四组,进行SAH出血量评级和小鼠神经功能缺陷评分,脑组织水含量测定脑水肿,伊文思蓝法测定血脑屏障(BBB)通透性,检测脑丙二醛(MDA)和谷胱甘肽(GSH)水平,神经核抗原(NeuN)和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记测定法(TUNEL)检测神经元存活和死亡率,WesternBlot检测脑凋亡相关斑点样蛋白(ASC)、白细胞介素-1β(IL-1β)、核苷酸结合寡聚化结构域样受体3炎症复合体(NLRP3)、B淋巴细胞瘤-2基因(Bcl2)、前凋亡因子(Bim)和活化的caspase-1蛋白表达,酶联免疫吸附测定(ELISA)脑中细胞因子白介素-1β(IL-1β)和白介素_6(IL-6)水平。结果槲皮素可以提高SAH小鼠生存率,降低神经功能缺陷评分,减少脑神经元凋亡,提高脑谷胱甘肽(GSH)水平,降低丙二醛(MDA)水平,减轻脑水肿和BBB通透性损害。槲皮素可以降低NLRP3以及细胞凋亡相关斑点样蛋白(ASC)的表达,抑制IL-1β、IL-6的分泌和活化的caspase-1的蛋白表达,并可以增高抗凋亡因子Bcl2的表达,降低凋亡前体因子Bim的表达。结论槲皮素通过抑制NLRP3炎性相关的凋亡来减轻SAH后的EBI。