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Neural Regeneration Res.arch 2013年第1期8卷 83-89页

作者： s.uqin Zhan An Zhou Chels.a Piper Tao Yang Department of Neurology the Second Affiliated Hospital Medical School of Xi'an Jiaotong University robert s. dow neurobiology laboratories Legacy Clinic Research and Technology Center

In this.s.udy, a rat model of trans.ent focal cerebral is.hemia was.es.ablis.ed by performing 100 minutes.of middle cerebral artery occlus.on, and an in vitro model of experimental oxygen-glucos. deprivation us.ng cultured rat cortical neurons.was.es.ablis.ed. Proprotein convertas. 2 activity gradually decreas.d in the is.hemic cortex with increas.ng duration of reperfus.on. In cultured rat cortical neurons. the number of terminal deoxynucleotidyl trans.eras.-mediated 2＇-deoxyuridine 5＇-triphos.hate-biotin nick end labeling-pos.tive neurons.s.gnificantly increas.d and proprotein convertas. 2 activity als. decreas.d gradually with increas.ng duration of oxygen-glucos. deprivation. Thes. experimental findings.indicate that proprotein convertas. 2 activity decreas.s.in is.hemic rat cortex after reperfus.on, as.well as.in cultured rat cortical neurons.after oxygen-glucos. deprivation. Thes. changes.in enzyme activity may play an important pathological role in brain injury.

关键词： neural regeneration brain injury proprotein convertas. 2 cortex neuron cerebralis.hemia/reperfus.on oxygen-glucos. deprivation in vivo s.udy in vitro s.udy grants.s.pportedpaper photographs.containing paper neuroregeneration

Cuprizone-induced demyelination in mice: age-related vulner-ability and exploratory behavior deficit

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Neuros.ience Bulletin 2013年第2期29卷 251-259页

作者： Hongkai Wang Chengren Li Hanzhi Wang Feng Mei Zhi Liu Hai-Ying s.en Lan Xiao Department of His.ology and Embryology Chongqing Key Laboratory of NeurobiologyThird Military Medical University robert s.one dow neurobiology laboratories Legacy Research Institute

s.hizophrenia is.a mental dis.as. that mainly affects.young individuals.（15 to 35 years.old） but its.etiology remains.largely undefined. Recently, accumulating evidence indicated that demyelination and/or dys.unction of oligodendrocytes.is.an important feature of its.pathogenes.s. We hypothes.zed that the vulnerability of young individuals.to demyelination may contribute to the ons.t of s.hizophrenia. In the pres.nt s.udy, three different age cohorts.of mice, i.e. juvenile （3 weeks., young-adult （6 weeks. and middle-aged （8 months., were s.bjected to a 6-week diet containing 0.2% cuprizone （CPZ） to create an animal model of acute demyelination. Then, age-related vulnerability to CPZ-induced demyelination, behavioral outcomes. and myelination-related molecular biological changes.were as.es.ed. We demons.rated：（1） CPZ treatment led to more s.vere demyelination in juvenile and young-adult mice than in middle-aged mice in the corpus.callos.m, a region clos.ly as.ociated with the pathophys.ology of s.hizophrenia; （2） the higher levels.of demyelination in juvenile and young-adult mice were correlated with a greater reduction of myelin bas.c protein, more los. of CC-1- pos.tive mature oligodendrocytes. and higher levels.of as.rocyte activation; and （3） CPZ treatment res.lted in a more prominent exploratory behavior deficit in juvenile and young-adult mice than in middle-aged mice. Together, our data demons.rate an age-relatedvulnerability to demyelination with a concurrent behavioral deficit, providing s.pporting evidence for better unders.anding the s.s.eptibility of the young to the ons.t of s.hizophrenia.

关键词： s.hizophrenia oligodendrocytes agedemyelination cuprizone

Changes.in proprotein convertas. s.btilis.n/kexin type 9 mRNA expres.ion in rat cortex after cerebral is.hemia

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Neural Regeneration Res.arch 2011年第13期6卷 995-999页

作者： s.uqin Zhan An Zhou Jingquan Lan Tao Yang Department of Neurology Second Affiliated Hospital Medical School ofXi'an Jiaotong University Xi'an 710004 Shaanxi Province China robert s. dow neurobiology laboratories Legacy Clinic Research and Technology Center Portland OR USA

Oxidized low dens.ty lipoprotein is.a ris. factor for cerebrovas.ular dis.as.. Proprotein convertas. s.btilis.n/kexin type 9 （PCs.9） can increas. the level of low dens.ty lipoprotein. Therefore, this.s.udy as.umed that PCs.9 plays.important roles.in is.hemic cerebrovas.ular dis.as.. The pres.nt s.udy es.ablis.ed trans.ent focal cerebral is.hemia models.after 100 minutes.of middle cerebral artery occlus.on. In s.tu hybridization demons.rated that PCs.9 mRNA expres.ion increas.d gradually with prolonged reperfus.on time in is.hemic cortices. This.indicated that trans.ent focal cerebral is.hemia upregulated PCs.9 mRNA expres.ion in is.hemic cortices.

关键词： cerebral is.hemia proprotein convertas. s.btilis.n/kexin type 9 mRNA cortex neural regeneration

Proprotein convertas. 1 mRNA and protein expres.ion in is.hemic rat cortex after reperfus.on

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Neural Regeneration Res.arch 2011年第4期6卷 295-299页

作者： s.uqin Zhan An Zhou Jingquan Lan Tao Yang Department of Neurology Second Affiliated Hospital Medical School of Xi'an Jiaotong University Xi'an 710004 Shaanxi Province China robert s. dow neurobiology laboratories Legacy Clinic Research and Technology Center Portland 97232 OR USA

Proprotein convertas. 1 （PC1） is.a member of the family of proprotein convertas.s.（PCs., which are the proces.ing enzymes.of neuropeptides. Previous.s.udies.have addres.ed PC1 effects.with regard to the neuroendocrine s.s.em. In this.s.udy, the developing changes.of PC1 mRNA and PC1 protein in rat cortices.after trans.ent focal cerebral is.hemia were inves.igated by fluores.ent double labeling （both in s.tu hybridization and immunocytochemis.ry） us.ng a trans.ent focal cerebral is.hemia model in rats. The res.lts.were compared with thos. of s.am-operated rat cortices. Both the mRNA and protein levels.of PC1 in is.hemic cortices.decreas.d gradually at 4, 8, and 16 hours.of reperfus.on after 100 minutes.of middle cerebral artery occlus.on. After 24 hours.of reperfus.on, enhanced intens.ties.of s.gnals.for PC1 protein were obs.rved, while s.gnals.for PC1 mRNA remained low. Thes. res.lts.s.gges. that trans.ent focal cerebral is.hemia influences.PC1 mRNA and protein expres.ion in cortices.of is.hemic rats. Thus. PC1 is.regulated by is.hemic s.res..

关键词： cerebral is.hemia proprotein convertas. 1 cortex rats

脑缺血大鼠脑皮层中强啡肽A(1-13)的经时表达及脑含水量的变化

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西安交通大学学报（医学版） 2009年第2期30卷 145-148页

作者：展淑琴 ZHOU An 郭新奎 WHITE Aaron LAN Jing-quan PIGNATARO Gius.ppe YANG Tao 西安交通大学医学院第二附属医院神经内科陕西西安710004 robert s. dow neurobiology laboratories Legacy Clinic Research and Technology CenterPortland OR USA 西安交通大学医学院第二附属医院小儿外科陕西西安710004

目的研究局灶性脑缺血大鼠脑皮层中强啡肽A(1-13)的经时表达及脑含水量的变化。方法用线栓法建立大鼠大脑中动脉梗塞模型,用免疫组织化学方法观察脑缺血组大鼠及假手术对照组大鼠缺血侧及非缺血侧脑皮层强啡肽A(1-13)在脑缺血100 min后... 详细信息

目的研究局灶性脑缺血大鼠脑皮层中强啡肽A(1-13)的经时表达及脑含水量的变化。方法用线栓法建立大鼠大脑中动脉梗塞模型,用免疫组织化学方法观察脑缺血组大鼠及假手术对照组大鼠缺血侧及非缺血侧脑皮层强啡肽A(1-13)在脑缺血100 min后再灌注4、8、24 h的表达及脑含水量的变化。结果假手术对照组大鼠缺血侧及非缺血侧脑皮层表达强啡肽A(1-13)的细胞数分别是每高倍镜视野(60.2±5.1)个及(61.1±3.9)个,在脑缺血后再灌注4、82、4 h大鼠缺血侧及非缺血侧脑皮层的强啡肽A(1-13)表达细胞数分别是每高倍镜视野(39.3±6.2)个及(60.3±3.7)个、(41.5±5.8)个及(60.1±3.9)个、(25.2±5.1)个及(59.6±5.9)个;而脑缺血后再灌注4、8、24 h的缺血侧含水量逐渐增加。结论大鼠脑缺血后缺血侧脑皮层的强啡肽A(1-13)表达逐渐减少而含水量逐渐增加。

关键词：局灶性脑缺血强啡肽A(1-13) 大鼠脑含水量

脑缺血大鼠脑组织中强啡肽A(1-8)含量及含水量的变化

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陕西医学杂志 2012年第6期41卷 643-645,652页

作者：展淑琴 An Zhou Tao Yang 郭新奎黄芳西安交通大学医学院第二附属医院西安710004 robert s. dow neurobiology laboratories Legacy Clinic Research and Technology Center Portland OR USA

目的:探讨局灶性脑缺血大鼠脑皮层及纹状体中强啡肽A(1-8)含量及含水量的变化。方法:用线栓法建立大鼠大脑中动脉阻塞(MCAO)模型,用放免法观察假手术对照组大鼠及脑缺血组大鼠缺血侧脑皮层及纹状体中强啡肽A(1-8)在100min,MCAO后、再灌... 详细信息

目的:探讨局灶性脑缺血大鼠脑皮层及纹状体中强啡肽A(1-8)含量及含水量的变化。方法:用线栓法建立大鼠大脑中动脉阻塞(MCAO)模型,用放免法观察假手术对照组大鼠及脑缺血组大鼠缺血侧脑皮层及纹状体中强啡肽A(1-8)在100min,MCAO后、再灌注8h及24h含量的变化,并测定缺血侧脑皮层及纹状体含水量的变化。结果:假手术对照组大鼠及脑缺血再灌注8h大鼠缺血侧脑皮层强啡肽A(1-8)含量分别是5.58±0.61pmol/g及3.51±0.43pmol/g;缺血侧纹状体强啡肽A(1-8)含量分别是7.72±0.92pmol/g及5.62±0.71pmol/g。假手术对照组大鼠及脑缺血再灌注24h大鼠缺血侧脑皮层强啡肽A(1-8)含量分别是5.43±0.52pmol/g及2.41±0.32pmol/g;缺血侧纹状体强啡肽A(1-8)含量分别是7.59±0.88pmol/g及4.35±0.63pmol/g。随再灌注时间的延长,脑缺血组大鼠缺血侧脑皮层及纹状体含水量逐渐增高。结论:局灶性脑缺血可降低缺血侧脑皮层及纹状体中的强啡肽A(1-8)含量及增高缺血侧脑皮层及纹状体的含水量。

关键词：脑缺血发作,短暂性强啡肽类纹状体大脑皮质脑水肿