β-淀粉样蛋白对大鼠海马星形胶质细胞N-甲基-D-天冬氨酸受体亚单位表达的影响

目的 探讨Wistar大鼠海马星形胶质细胞N-甲基-D-天冬氨酸受体（NMDAR）亚单位在β-淀粉样蛋白（Aβ）25~35毒性作用下的表达变化特点。方法 大鼠海马原代培养细胞,加Aβ _25~35（10μmol/L）分别作用1h、24h后,应用免疫荧光方法检测对照组和加药组中NR1、NR2A和NR2B的表达情况（n =10）。 结果 对照组海马星形胶质细胞表达NR1、NR2A和NR2B,阳性点状颗粒主要分布在细胞胞体和突起上,在胞体部位分布密集,在细胞突起则散在分布。经Aβ _25~35作用后,三者表达均显著增强（ P <0．05)。Aβ1h组和24h组相比,NR1无显著变化,NR2A、NR2B的表达随作用时间增加显著增强（　P　<0．05)。结论　正常状态下海马星形胶质细胞可表达NMDAR亚单位（NR1、NR2A和NR2B);Aβ _25~35作用会引起NMDAR各亚单位表达显著增强,NR1的表达变化与NR2A和NR2B的变化表现出不一致性。     

母源性甲状腺功能亢进对仔鼠心脏甲状腺激素受体mRNA表达的影响

目的 探讨母源性甲状腺功能亢进（简称甲亢）对新生仔鼠心脏中甲状腺激素受体的影响。方法 首先对24只雌性Wistar大鼠建立妊娠合并甲亢模型,取新生5d、10d、15d仔鼠心脏进行解剖检查,取部分心脏组织石蜡切片Masson染色,取部分心脏组织采用实时定量PCR法检测甲
状腺激素受体（TR）α₁、TRα₂、TRβ₁ mRNA水平表达量的变化。结果 在心脏组织中TRα1 mRNA的表达量较TRα₂、TRβ₁的表达量高,且在出生10d的仔鼠心脏（包括甲亢组和对照组）中TRα₁mRNA的表达量呈现峰值;与同期对照仔鼠相比,母源性甲亢仔鼠出生5d 与出生10d心肌中TRα₁
mRNA的表达量显著上调,出生15d的表达量与对照组相比表达量下调;TRα₂在母源性甲亢和对照中差异无统计学意义;TRβ₁在甲亢出生5d仔鼠中表达量显著下调,10d组表达量上调,15d组表达量差异无显著性。结论 母源性甲亢会对仔鼠心肌产生影响,引起甲状腺激素受体的差异表达;
这种变化随出生后时间延长而减弱。甲状腺激素受体中TRα₁的变化最显著,可能在甲亢引起的心肌损伤中起重要作用。     

有氧运动干预Aβ1-42诱导阿尔茨海默病大鼠海马突触结构与突触蛋白的改变

背景：β-淀粉样蛋白(Aβ)在海马中的积累和沉积会影响突触形态和功能,导致突触可塑性受损,后者被认为是阿尔茨海默病学习记忆缺陷的根本原因。有氧运动能否减轻淀粉样蛋白诱导的突触受损从而改善阿尔茨海默病患者的学习记忆能力尚不清楚。目的：观察有氧运动对Aβ_1-42诱导阿尔茨海默病大鼠海马突触结构与突触标志性蛋白突触素、突触后致密物95表达的影响,探讨有氧运动对阿尔茨海默病学习记忆能力影响的机制。方法：将80只SD大鼠随机分为4组,即生理盐水对照组、生理盐水运动组、Aβ_1-42诱导模型组以及Aβ_1-42运动组,每组20只。其中后两组大鼠双侧海马注入10μL Aβ_1-42(1μg/μL),前两组大鼠双侧海马注入10μL生理盐水。Aβ_1-42/生理盐水注射后第2天,生理盐水运动组和Aβ_1-42运动组开始进行有氧运动训练,持续5周,每周运动6 d。采用Morris水迷宫实验检测大鼠学习记忆能力,然后取脑组织,采用电镜技术及免疫荧光、Western blot技术分别检测大...     

Sonic hedgehog信号通路在单侧输尿管梗阻大鼠肾组织中的表达变化及意义

 目的：探讨Sonic hedgehog（Shh）信号通路在单侧输尿管梗阻（UUO）大鼠肾组织中的表达变化及意义。方法：将48只SD大鼠随机分为UUO模型组（n=24）和假手术组（n=24）,梗阻术3、7和14 d后取其梗阻侧肾脏组织。用HE和Masson染色检测肾间质纤维化程度,免疫组织化学染色检测Shh通路分子Shh、Ptch1、Smo、Gli1及III型胶原的蛋白表达,酶联免疫吸附实验（ELISA）检测肾组织中TGF-β₁和Shh含量,real-time RT-PCR检测TGF-β₁、I和III型胶原及Shh通路分子mRNA表达。结果：HE和Masson染色显示,梗阻侧肾组织出现明显的纤维化病变,且随时间延长而加剧。TGF-β₁、I和III型胶原含量在梗阻肾中表达明显增高（P<0.05）。同时,Shh信号通路分子Shh、Smo和Gli mRNA和蛋白在梗阻肾中表达明显升高（P<0.05）,而Ptch1 mRNA和蛋白的表达下调（P<0.01）,提示Shh信号被激活。相关分析表明,Shh信号起始信号Shh水平的升高与TGF-β₁含量增加呈明显的相关。结论：UUO大鼠诱导肾间质纤维化发生过程中,Shh信号通路分子被激活,推测可能的机制是活化的Shh信号通路诱导TGF-β₁表达和释放,导致肾间质纤维化。     

HSP90通过PTK2B影响Aβ1-42诱导的痴呆小鼠学习记忆功能

目的:探讨热休克蛋白90(HSP90)和蛋白酪氨酸激酶2β(PTK2B)与Aβ_1-42诱导痴呆模型小鼠学习记忆功能的关系。方法:32只C57BL/6J小鼠分为对照组(NS)、痴呆模型组(Aβ_1-42+NS)、HSP90抑制剂Luminespib处理组(Aβ_1-42+Lum)以及PTK2B抑制剂PF431396处理组(Aβ_1-42+PF)。实验组侧脑室注射Aβ_1-42构建痴呆模型后分别注射HSP90抑制剂或PTK2B抑制剂进行处理。采用水迷宫对小鼠学习记忆功能进行检测，Western Blot检测海马HSP90、PTK2B的表达情况以及tau蛋白磷酸化水平(p-tau),免疫组织化学染色检测海马HSP90和PTK2B的表达，real time RT-PCR检测PTK2B mRNA表达。结果:在Aβ_1-42诱导的痴呆模型小鼠海马中，PTK2B及p-tau水平均升高，HSP90水平降低(P<0.01)。而应用HSP90抑制剂则更进一步导致小鼠海马PTK2B...     

阿魏酸钠通过Notch1/Hes信号通路对抗Aβ1-42引起的SD胎鼠海马神经元凋亡

目的 探讨阿魏酸钠(Sodium ferulate, SF)对Aβ_1-42引起的SD胎鼠海马神经元凋亡的抑制作用及相关机制。方法 原代培养海马神经元,选取培养8 d的成熟细胞,分为以下四组：对照组(Control,加入0.1%DMSO作用72 h);Aβ_1-42组(加入终浓度50 nmol/LAβ_1-42作用72 h);SF+Aβ_1-42组(先加入200μmol/LSF作用6h后再加入Aβ_1-42);SF+Aβ_1-42+Jagged1组(Jagged1为Notch1/Hes信号通路激动剂,先加入200μmol/LSF和400μg/L Jagged1作用6 h后再加入Aβ_1-42)。MTT检测细胞活力,TUNEL染色及流式细胞仪检测细胞凋亡情况,Western blot检测各组细胞Notch1、Hes、Bax及Bcl-2蛋白相对表达。结果 与Control组相比,Aβ_1-42组和SF+Aβ_1-42     

转化生长因子β1降低大鼠自发性癫痫发作并抑制胶质细胞活化

 目的：观察经鼻给予转化生长因子β₁（TGF-β₁）是否能减少匹罗卡品致痫大鼠慢性自发性癫痫的发作并探讨其可能机制。方法：经鼻给予大鼠重组人TGF-β₁或等量PBS溶液,以匹罗卡品建立癫痫持续状态模型,癫痫持续状态后7 d经动态视频记录其活动,通过胶质纤维酸性蛋白(GFAP)和离子钙结合接头分子1（Iba1）免疫组化观察癫痫大鼠海马组织胶质细胞的活化,采用尼氏染色观察海马区神经元的死亡。结果：TGF-β₁有效降低自发性癫痫的平均频率、发作程度和持续时间。癫痫持续状态后14 d TGF-β₁治疗组海马区活化的胶质细胞明显少于匹罗卡品模型组（P<0.05）;TGF-β₁显著降低海马CA3区神经元的死亡(P<0.01)。结论：经鼻给予TGF-β₁可降低大鼠自发重复性癫痫发作,抑制胶质细胞活化,从而减少神经元的死亡。     

自噬标志物LC3的节律表达破坏参与β1-AA诱导的H9c2大鼠心肌细胞死亡

目的:探讨β₁-肾上腺素受体(β₁-AR)自身抗体(β₁-AA)对大鼠心肌细胞自噬标志物微管相关蛋白1轻链3(LC3)节律表达的影响及其在心肌细胞死亡中的作用。方法:实验材料为Sprague-Dawley(SD)大鼠和H9c2大鼠心肌细胞。将SD大鼠随机分为免疫组(β₁-AR组)和对照(control)组,每组6只;将H9c2细胞随机分为control组、β₁-AA组、慢病毒(LV)-NC组和LV-shPer2组(n=6);合成β₁-AR细胞外第二环抗原肽段,用于主动免疫大鼠,并使用亲和层析法从大鼠血清中提纯β₁-AA;β₁-AA处理H9c2细胞24 h后使用CCK-8法检测细胞活力;用地塞米松同步化细胞后,再给予β₁-AA处理,采用real-time PCR及Western blot法检测LC3的表达情况,采用Western blot法检测生物钟蛋白Per2的表达情况,使用JTK_CYCLE算法分析昼夜节律参数;用LV-shPer2感染H9c2细胞以破坏LC3的节律表达,进而采用CCK-8法检测细胞活力。结果:β₁-AR组大鼠血清中β₁-AA的A值与control组相比显著升高(P<0.05)。β₁-AA组H9c2细胞的活力显著低于control组(P<0.05)。β₁-AA可破坏H9c2细胞LC3和Per2的节律表达(JTK_CYCLE P<0.05)。通过LV-shPer2干扰Per2基因而破坏H9c2细胞LC3节律表达(JTK_CYCLE P<0.05)后,细胞活力显著降低(P<0.05)。结论:β₁-AA破坏H9c2大鼠心肌细胞自噬标志物LC3的节律表达,从而促进细胞死亡。     

CircRNA_23113抑制肺腺癌细胞的增殖和迁移

目的探究circRNA₂3113在肺腺癌中的表达及对肺腺癌细胞增殖和迁移的影响。方法通过高通量测序技术测序5例临床肺腺癌、癌旁组织标本,筛选出差异性表达的circRNA₂3113。实时荧光定量PCR检测肺腺癌组织、血清和细胞中circRNA₂3113的表达;构建circRNA₂3113的过表达质粒,用CCK-8法、克隆形成实验、细胞划痕和Transwell小室法分析其对细胞增殖和迁移的影响;用Western blot检测β-catenin、cyclin D1以及c-myc蛋白水平的表达。结果 CircRNA₂3113在肺腺癌患者组织、血清和细胞中显著低表达（P<0.05）;过表达circRNA₂3113后抑制A549和H1299细胞增殖和迁移（P<0.05）;CircRNA₂3113抑制β-catenin、cyclin D1以及c-myc表达（P<0.05）。结论 CircRNA₂3113在肺腺...     

Bak基因转染对乳腺癌MCF-7细胞增殖及对紫杉醇敏感性的影响

目的 探讨Bak基因转染对乳腺癌MCF-7细胞增殖及对紫杉醇敏感性的影响。 方法 采用Western blotting法和Real-time PCR检测乳腺癌MCF-7细胞转染前后Bak蛋白表达。通过细胞计数试剂盒8（CCK-8）和流式细胞术检测Bak基因转染后,及紫杉醇作用24 h、48 h和72 h后对MCF-7细胞增殖和细胞周期的影响。 结果 Western blotting和 Real-time PCR检测结果显示,转染质粒后,Bak蛋白表达量显著升高,MCF-7 Bak组mRNA表达量为2.15±0.07,明显高于MCF-7 NC组1.03±0.04（t=13.412,P<0.05）。转染48 h、72 h和96 h后,MCF-7 Bak细胞增殖速率为（0.31±0.03）%、（0.37±0.03）%、（0.47±0.04）%,低于MCF-7 NC组的（0.40±0.03）%、0.48±0.04）%、（0.61±0.06）%,差异有统计学意义（t ₄₈=2.145、t ₇₂=3.164、t ₉₆=5.487,P<0.05）。MCF-7 Bak组G2期细胞数是（26.84±2.69）%,显著高于MCF-7 NC组（16.02±1.61）%（t=12.887,P<0.05）。紫杉醇作用24 h、48 h和72 h后,MCF-7 Bak组细胞增殖抑制率为（35.98±4.00）%、（54.66±5.50）%、（80.11±8.00）%,高于MCF-7 NC组的（24.12±2.40）%、（40.12±4.00）%、（61.09±6.09）%,差异有统计学意义（t ₂₄=8.456、t ₄₈=10.547、t ₇₂=13.442,P<0.05）。紫杉醇作用24 h后,MCF-7 Bak组G0/G1期细胞数（73.01±7.02）%高于MCF-7 NC组（63.84±6.68）%（P<0.05）。 结论 上调Bak基因表达可抑制乳腺癌MCF-7细胞增殖,上调G0/G1期比例,增强紫杉醇的敏感性。     

甘氨酸受体α_1亚基在乳鼠心肌细胞的表达及损害性因素对其表达的影响

目的:研究甘氨酸受体α1亚基(GlyRα1)在乳鼠心肌细胞中的表达以及脂多糖(LPS)、缺氧/复氧(H/R)、异丙肾上腺素(ISO)和高糖(HG)对其表达的影响。方法:体外培养乳鼠心肌细胞,Western blotting方法检测心肌细胞上GlyRα1的表达;心肌细胞分别用LPS、H/R、ISO以及HG处理24 h,采用CCK-8试剂检测细胞活力,Western blotting方法检测心肌细胞上GlyRα1的表达。结果:Western blotting方法检测到乳鼠心肌细胞上GlyRα1的表达;LPS(20 mg/L)、ISO(100μmol/L)以及HG(25mmol/L)处理心肌细胞24 h与心肌细胞H/R 3 h对心肌细胞存活率无明显影响;LPS组、H/R 3 h组以及ISO组心肌细胞上GlyRα1表达均高于对照组(P0.01),而HG组心肌细胞上GlyRα1表达低于对照组(P0.01)。结论:乳鼠心肌细胞上存在GlyRα1,并且一定浓度的LPS、ISO与一定时间的H/R均可上调乳鼠心肌细胞GlyRα1的表达,而HG可下调乳鼠心肌细胞GlyRα1的表达。     

Distribution of N-methyl-D-aspartate receptors (NMDARs) in the developing rat brain

The N-methyl-D-aspartate receptor (NMDAR), which is one of the glutamate receptors, is considered to have a close relationship to synaptic plasticity in the developing brain. In addition, it is known that the excessive stimulation of NMDARs can trigger neuronal apoptosis. In this study, we examined the distribution of NMDAR subunits [anti-NR1, NR2(A-C)] in the developing rat brain immunohistochemically. As a result, NR1, an essential subunit for the formation of a functional NMDAR complex, was mildly expressed in the restricted areas such as the temporal region of the cerebral cortex and the hippocampus in the fetal brain at Embryonal Days 18 and 20. On the other hand, in neonates, NR1 was expressed widely throughout the whole brain. The distributions of NR2A and NR2C showed temporal and spatial similarities to that of NR1, while the expression of NR2B showed differences in the intensity and distribution. A progressive change in subunit expression seen prenatally and postnatally could contribute to variation of NMDARs and synaptic plasticity during the developing period.     

Dark-rearing decreases NR2A N-methyl-D-aspartate receptor subunit in all visual cortical layers

Maturation of the visual cortex is a visual experience-dependent process. It has been shown that visual input triggers changes in N-methyl-D-aspartate receptor (NMDAR) subunit expression in the visual cortex. However, no data are available on the layer distribution of these molecular changes. Here we describe the laminar distribution of the cells expressing the NMDAR subunits NR2A and NR2B in the rat primary visual cortex at postnatal day (P) 21 and 37 using anti-NR2A and anti-NR2B antibodies and a stereological method to count labelled neurons. The percentage of neurons expressing the NR2A subunit in the layers II-VI remained unchanged between P21 and P37 with a slight decrease in layer V. Dark-rearing from P21 to P37 induced a pronounced decrease of the staining intensity and a significant decrease in the percentage of NR2A-expressing neurons. The changes in NR2A expression caused by dark rearing occur at similar levels in layers II-VI. The percentage of NR2B-positive cells in the different cortical layers remains unchanged from P21 to P37. The NR2B pattern was not significantly affected by dark-rearing. Thusly, the expression of NR2A depends upon visual experience after P21.     

Circadian and developmental regulation of N-methyl-d-aspartate-receptor 1 mRNA splice variants and N-methyl-d-aspartate-receptor 3 subunit expression within the rat suprachiasmatic nucleus

The circadian rhythms of mammals are generated by the circadian clock located in the suprachiasmatic nucleus (SCN) of the hypothalamus. Its intrinsic period is entrained to a 24 h cycle by external cues, mainly by light. Light impinging on the SCN at night causes either advancing or delaying phase shifts of the circadian clock. N-methyl-d-aspartate receptors (NMDAR) are the main glutamate receptors mediating the effect of light on the molecular clockwork in the SCN. They are composed of multiple subunits, each with specific characteristics whose mutual interactions strongly determine properties of the receptor. In the brain, the distribution of NMDAR subunits depends on the region and developmental stage. Here, we report the circadian expression of the NMDAR1 subunit in the adult rat SCN and depict its splice variants that may constitute the functional receptor channel in the SCN. During ontogenesis, expression of two of the NMDAR1 subunit splice variants, as well as the NMDAR3A and 3B subunits, exhibits developmental loss around the time of eye opening. Moreover, we demonstrate the spatial and developmental characteristics of the expression of the truncated splice form of NMDAR1 subunit NR1-E in the brain. Our data suggest that specific properties of the NMDAR subunits we describe within the SCN likely influence the photic transduction pathways mediating the clock entrainment. Furthermore, the developmental changes in NMDAR composition may contribute to the gradual postnatal maturation of the entrainment pathways.     

Neuroexcitatory targets in the female reproductive system of the nonhuman primate (Macaca fascicularis)

Glutamate receptors (GluRs) have been implicated in brain function and pathology. Their presence in peripheral tissues suggests a vital role in the pathophysiology of various organ systems. In earlier studies, the authors reported the differential distribution of ionotropic and metabotropic GluRs in neural and nonneural peripheral tissues of the rat. In this study, they investigated the presence and the localization of the GluRs in the reproductive organs of Macaca fascicularis. The data illustrate the presence of the GluR 2/3, metabotropic glutamate receptor 2/3, kainate 2, and N-methyl-D-aspartate receptor 1 (NMDAR 1). These are localized in the different structures of the ovaries, uterine cervix, myometrium, endometrium, and inflammatory cells. Smooth muscle of the myometrium and arterioles showed strong immunolabeling with anti-GluR 2/3 and, to a lesser intensity, with the other ionotropic glutamate receptor antibodies. NMDAR 1 showed the most widespread staining in all the structures. Mast cells showed strong immunolabeling with the anti-NMDA antibody. The demonstration and the differential expression of GluRs in the female reproductive system of nonhuman primate experimental models provide first evidence suggesting excitatory signaling in these tissues.     

Role of the NR2A/2B subunits of the N-methyl-D-aspartate receptor in glutamate-induced glutamic acid decarboxylase alteration in cortical GABAergic neurons in vitro

The vulnerability of brain neuronal cell subpopulations to neurologic insults varies greatly. Among cells that survive a pathological insult, for example ischemia or brain trauma, some may undergo morphological and/or biochemical changes that may compromise brain function. The present study is a follow-up of our previous studies that investigated the effect of glutamate-induced excitotoxicity on the GABA synthesizing enzyme glutamic acid decarboxylase (GAD65/67)'s expression in surviving DIV 11 cortical GABAergic neurons in vitro [Monnerie and Le Roux, (2007) Exp Neurol 205:367-382, (2008) Exp Neurol 213:145-153]. An N-methyl-D-aspartate receptor (NMDAR)-mediated decrease in GAD expression was found following glutamate exposure. Here we examined which NMDAR subtype(s) mediated the glutamate-induced change in GAD protein levels. Western blotting techniques on cortical neuron cultures showed that glutamate's effect on GAD proteins was not altered by NR2B-containing diheteromeric (NR1/NR2B) receptor blockade. By contrast, blockade of triheteromeric (NR1/NR2A/NR2B) receptors fully protected against a decrease in GAD protein levels following glutamate exposure. When receptor location on the postsynaptic membrane was examined, extrasynaptic NMDAR stimulation was observed to be sufficient to decrease GAD protein levels similar to that observed after glutamate bath application. Blocking diheteromeric receptors prevented glutamate's effect on GAD proteins after extrasynaptic NMDAR stimulation. Finally, NR2B subunit examination with site-specific antibodies demonstrated a glutamate-induced, calpain-mediated alteration in NR2B expression. These results suggest that glutamate-induced excitotoxic NMDAR stimulation in cultured GABAergic cortical neurons depends upon subunit composition and receptor location (synaptic vs. extrasynaptic) on the neuronal membrane. Biochemical alterations in surviving cortical GABAergic neurons in various disease states may contribute to the altered balance between excitation and inhibition that is often observed after injury.     

N-methyl-d-aspartate receptor subunit expression in adult and adolescent brain following chronic ethanol exposure

Substantial evidence suggests that glutamatergic neurotransmission is a critical mediator of the experience-dependent synaptic plasticity that may underlie alcohol dependence. Substance abuse typically begins in adolescence; therefore, the impact of alcohol on glutamatergic systems during this critical time in brain development is of particular importance. The N-methyl-d-aspartate receptor (NMDAR) is involved in developmental mechanisms underlying neuronal differentiation and synaptogenesis and as such may be a target system for alcohol effects during adolescence. In the present study quantitative biochemical determinations were made of the relative abundance of different protein expressions of NMDAR subunits in adolescents and adults after 2 weeks of ethanol vapor exposure, and 24 h and 2 weeks following withdrawal. After 2 weeks of ethanol vapor exposure N-methyl-d-aspartate receptor NR1 subunit (NR1), N-methyl-d-aspartate receptor NR2A subunit (NR2A), and N-methyl-d-aspartate receptor NR2B subunit (NR2B) subunit expression was found to be increased in hippocampus of the adults. In contrast, 2 weeks of ethanol exposure resulted in no significant changes in NR1 and NR2B subunits and a reduction NR2A subunit expression in hippocampus in adolescents. Twenty-four h and 2 weeks following withdrawal from ethanol vapor NR1 and NR2A subunit expression in hippocampus was decreased in adolescents, whereas in adults it had returned to control levels. In frontal cortex, 2 weeks of chronic ethanol exposure produced decreases in NR1 subunit expression in both adults and adolescents but also produced decreases in NR2A and NR2B subunit expression in adults that returned or exceeded control levels by 2 weeks following withdrawal from ethanol vapor. These results demonstrate that NMDAR subunit composition can be modulated differentially between adolescents and adults by chronic ethanol exposure and withdrawal. These developmental differences in NMDAR subunits composition may also be associated with the enhanced vulnerability of the adolescent brain to ethanol dependence.     

缺氧缺血对O-2A祖细胞膜铁转运蛋白1表达的影响

目的 观察膜铁转运蛋白1（FPN1）在O-2A祖细胞缺氧缺血损伤后的表达变化,探讨其在O-2A祖细胞缺氧缺血损伤中的作用。方法 体
外培养O-2A祖细胞,以特异性抗体A2B5鉴定,观察FPN1在O-2A祖细胞上的定位表达;以糖氧剥夺（OGD）法建立缺氧缺血细胞模型,CCK8法检测
细胞存活率;应用免疫荧光染色法、实时荧光定量PCR法和Western blotting法观察FPN1在细胞缺氧缺血后的表达变化。结果 FPN1定位表达于
O-2A祖细胞的细胞膜、细胞质和突起;OGD3h、6h、12h及24h细胞存活率呈时间依赖性降低（P＜0.05）;OGD12h内细胞FPN1免疫荧光强度进行
性减弱;与OGD0h相比,FPN1 mRNA和蛋白水平在OGD3h表达下调,OGD6h进一步降低,OGD12h最低,差异具有统计学意义（P＜0.05）。结论 O-2A
祖细胞缺氧缺血损伤后FPN1表达明显下调,细胞存活率显著降低,提示FPN1可能参与O-2A祖细胞的缺氧缺血损伤过程。     

轴突损伤对大鼠球海绵体肌脊核内运动神经元NMDA受体亚单位表达的影响

本研究观察了轴突损伤对大鼠球海绵体肌脊核(SNB)内运动神经元离子型谷氨酸受体亚单位NMDAR1、NMDAR2A和NMDAR2B表达的影响。实验用雄性SD大鼠,切断单侧阴部神经,动物分别存活1、3、7、14或21d后,进行免疫组织化学染色及定量分析。结果显示正常大鼠SNB内运动神经元表达NMDAR1、NMDAR2A和NMDAR2B亚单位,其中NMDAR2B染色密度最高,NMDAR1次之,NMDAR2A染色密度最低;轴突损伤导致同侧SNB内运动神经元NMDA受体亚单位表达改变,其中NMDAR1染色密度降低,NMDAR2B染色密度增高,而NMDAR2A保持不变。轴突损伤后第3d受体染色密度变化明显,第7d达高峰,第21d恢复近正常水平。本文结果提示,SNB内运动神经元NMDA受体亚单位对轴突损伤呈现不同的反应,这可能与受损运动神经元的存活与再生有关。