重组人粒细胞集落刺激因子增加脑缺血周边区纤维结合蛋白的表达

目的:验证重组人粒细胞集落刺激因子(rhG-CSF)是否能改善局灶性脑缺血大鼠的神经功能,并观察纤维结合蛋白表达。方法:线栓法复制大鼠大脑中动脉梗塞模型,皮下注射rhG-CSF,10μg·kg^-1·d^-1,连续5d。进行神经功能缺损评分。采用免疫组织化学方法观察纤维结合蛋白以及5溴-2脱氧尿苷(Brdu)的表达。运用免疫荧光双标法,观察缺血周边区Brdu和纤维结合蛋白以及神经胶质元纤维酸性蛋白(GFAP)和纤维结合蛋白的双阳性表达。结果:①手术7d、14d、21d干预组的神经功能缺损评分分别为4.00±0.89、3.83±1.17、3.50±1.38,手术对照组分别为5.50±1.38、5.83±1.47、5.66±1.63,手术干预组明显低于手术对照组(P<0.05);②手术干预组缺血周边区的纤维结合蛋白和Brdu免疫阳性细胞数均明显多于手术对照组(P<0.05);③手术组缺血周边区见Brdu和纤维结合蛋白以及GFAP和纤维结合蛋白的双阳性细胞;④手术干预组缺血周边区的血管周围可见簇状分布的纤维结合蛋白免疫阳性细胞。结论:rhG-CSF可增加脑缺血之后缺血周边区纤维结合蛋白的表达和改善神经功能。     

孕鼠宫颈注射脂多糖对仔鼠脑细胞GFAP、MBP表达的影响

目的： 研究脂多糖致宫内感染仔鼠脑细胞中胶质纤维酸性蛋白（glial fibrillary acidic protein,GFAP）、髓鞘碱性蛋白(myelin basic protein,MBP)含量的变化以及对仔鼠脑重和体重发育的影响。方法: 经宫颈在受孕第10 d（E10组）、15 d（E15组）和20 d（E20组）注射脂多糖建立宫内感染模型,于仔鼠出生后7 d、14 d和21 d断头取脑,测量脑重和体重。采用免疫组化法测定GFAP、MBP含量。结果: 脂多糖致宫内感染后仔鼠脑组织中GFAP和MBP的含量逐步增高（P<0.01,P<0.05）,且21 d组GFAP明显高于7 d组（P<0.01）、21 d组MBP高于7d组（P<0.05）。感染后仔鼠的体重大于对照组（P<0.05）,而生后7 d和14 d仔鼠的脑重大于对照组（P< 0.01,P<0.05）。结论: 脂多糖致宫内感染可导致仔鼠脑细胞GFAP、MBP含量升高。     

脂肪来源的干细胞移植对脑缺血大鼠神经轴突再生的影响

目的:探讨脂肪来源的干细胞(ADSC)移植对脑缺血大鼠神经轴突生长以及神经胶质酸性蛋白(GFAP)、神经突蛋白(Neuritin)、神经微丝蛋白200(NF-200)表达的影响。方法:54只清洁级成年雄性SD大鼠,随机分为3组:假手术组(Sham组)、模型组(MCAO组)及MCAO+ADSC治疗组(ADSC组),每组18只。采用改良Zea-Longa线栓制法大脑中动脉栓塞(MCAO)模型,ADSC移植前用DAPI标记,ADSC组于造模成功1 d后经侧脑室注射入ADSC(1×106),分别于术后7 d、14 d、28 d观察其恢复情况,并断头取脑,通过免疫荧光、Western blot法检测脑缺血组织中GFAP、Neuritin、NF-200表达情况。结果:ADSC组缺血周边区脑组织中能观察到DAPI染色的阳性细胞;ADSC组与MCAO组相比在各个时间点脑组织中GFAP阳性细胞表达明显降低(P<0.05),神经突蛋白和神经微丝蛋白200表达明显增高(P<0.05)。结论:ADSC移植后可引起脑缺血后期组织中Neuritin、NF-200有效表达,并抑制GFAP阳性细胞增生,促进了神经轴突再生和修复。     

脑室周围白质软化大鼠膜铁转运蛋白1的表达变化及意义

目的:探讨缺氧缺血脑室周围白质软化(PVL)大鼠膜铁转运蛋白1(FPN1)的表达变化及意义.方法:新生4日龄SD大鼠随机分为对照组和缺氧缺血PVL组,于术后1d、3d、1周和4周取脑,分离大脑皮质、海马和脑室周围白质,以石墨炉原子吸收分光光度法检测各脑区铁含量,应用免疫荧光组织化学显色观察FPN1蛋白定位,应用实时荧光定量PCR和免疫印迹分别检测FPN1 mRNA与蛋白表达水平.结果:与对照组相比,PVL组各脑区铁含量于术后1d与3d无增加；术后1周均较对照组增高,其中以脑室周围白质铁含量增加最显著,皮质次之,海马最少；术后4周皮质铁含量略有降低,海马铁含量已降至对照组水平,而脑室周围白质铁含量仍处于高水平.PVL组各脑区FPN1 mRNA和蛋白于术后1d与3d未见明显变化；术后1周均较对照组明显降低；术后4周皮质FPN1表达量有所恢复,海马FPN1已恢复至对照组水平,但脑室周围白质FPN1仍较对照组降低.结论:缺氧缺血PVL大鼠皮质、海马与脑室周围白质铁含量升高,而FPN1的表达减少,两者均呈时空依赖性.提示新生4日龄SD大鼠缺氧缺血后FPN1表达减少可能引起脑铁升高,促进PVL的发生.     

宫内感染致脑损伤对仔鼠认知发育和海马神经发生的影响

 目的:探讨宫内感染致仔鼠脑损伤后对认知发育和海马神经发生的影响。方法: 15只Sprague-Dawley孕鼠（孕15 d）按随机数字表法分为造模组（8只）和对照组（7只）。繁殖后的2组雄性仔鼠按随机数字表法分为宫内感染组（35只）和对照组（35只），进行大脑解剖学观察、神经细胞凋亡检测、Morris水迷宫实验、神经细胞增殖及存活分析。结果: （1）宫内感染组仔鼠大脑较对照组萎缩，TUNEL阳性细胞数和caspase-3阳性细胞数均较对照组显著增加 (P<0.05)。（2）宫内感染组仔鼠近期记忆及远期记忆保持能力均较对照组降低，潜伏期显著延长（P<0.05）。（3）细胞增殖分析显示宫内感染组3 、7 和14日龄仔鼠BrdU阳性细胞数较对照组显著增加（P<0.05）；细胞存活分析显示，28日龄的2组仔鼠BrdU阳性细胞数无显著差异（P>0.05）。结论: 宫内感染可致仔鼠脑损伤，海马神经细胞凋亡可能与认知发育障碍密切相关。宫内感染诱导的神经发生可能与脑损伤后神经自身修复有关。     

MCT1在不同发育时期及缺血缺氧脑白质损伤大鼠胼胝体内的表达

目的:观察单羧酸转运体-1(monocarboxylate transporter-1,MCT1)在不同发育时期及缺血缺氧(hypoxia-ischemia,HI)损伤模型大鼠胼胝体内的表达。方法:采用多聚甲醛灌注固定7 d、14 d、21 d和28 d SD大鼠脑组织,冰冻切片后进行MCT1/CNPase和MCT1/GFAP免疫荧光双标,观察胼胝体内MCT1在少突胶质细胞和星形胶质细胞的表达;另选生后3 d的SD大鼠,右侧颈总动脉结扎及缺氧处理以建立HI性脑白质损伤模型,至生后28d观察胼胝体MCT1的表达。结果:MCT1分别与CNPase和GFAP免疫荧光双标显示,生后早期,正常大鼠胼胝体内MCT1主要在GFAP阳性细胞表达,随生长时间延长,MCT1在CNPase阳性细胞的表达增加,而在GFAP阳性细胞的表达逐渐减少;HI损伤后28 d,MCT1/GAFP免疫荧光强度较对照组显著升高(P0.01),而MCT1/CNPase的表达较对照组显著降低(P0.01)。结论:在成年SD大鼠胼胝体,MCT1主要在CNPase阳性的少突胶质细胞表达,而HI脑白质损伤后,MCT1主要在星形胶质细胞表达。     

川芎嗪对大鼠脑缺血再灌注损伤后GFAP表达和脑组织水肿的影响

探讨川芎嗪对大鼠脑缺血再灌注损伤后星形胶质细胞表达胶质原纤维酸性蛋白(GFAP)以及对脑组织含水量的影响。将70只SD大鼠随机分为3组:脑缺血后1、3、5、7、10d模型组(n=30,每个时间点用6只)、川芎嗪预处理组(n=30,每个时间点用6只)和假手术组(n=10,每个时间点用2只)。采用线栓法制作大鼠局灶性脑缺血再灌注模型(MCAO),应用免疫组化法观察星形胶质细胞GFAP的表达,干湿重法测定脑组织的含水量。结果显示:川芎嗪预处理组大鼠各时间点海马CA1区的GFAP阳性细胞数量显著增多,与缺血模型组比较均有显著性差异(P<0.05)。缺血再灌注后脑组织含水量持续性增加,到3d达到最高峰,5d时仍较高,以后逐渐降低;川芎嗪组各时间点的脑组织含水量均低于缺血模型组(P<0.05)。上述研究结果提示川芎嗪可引起星形胶质细胞活化、保护神经元、减轻脑水肿,具有防治脑缺血再灌注损伤的作用。     

银杏叶提取物对局灶性脑缺血再灌注不同时段的大鼠脑组织GFAP的影响

目的观察银杏叶提取物(extract of Ginkgo biloba,EGB)对大鼠局灶性脑缺血再灌注梗死区胶质纤维酸性蛋白(GFAP)表达的影响。方法采用改良线栓法建立大鼠大脑中动脉阻塞脑缺血再灌注模型。观察再灌注1～4d里大鼠神经功能缺损程度并应用免疫组织化学法、Metamoph图像分析系统对结果进行分析。结果EGB药物组神经功能评分较缺血再灌组好(P<0.05),GFAP阳性细胞于脑缺血2h再灌注24h后即已出现,48、72、96h阳性细胞表达量增加,其中以72h为最多,EGB可抑制缺血后GFAP的表达(P<0.05)。结论局灶性脑缺血后可诱导脑组织GFAP表达增强,EGB可抑制脑缺血再灌注后星形胶质细胞GFAP的高表达,提示EGB对缺血诱导的星形胶质细胞活化具有抑制作用,可能对脑缺血损伤的恢复起重要作用。     

人参皂苷Rbl对大鼠局灶性脑缺血白质重塑的影响

目的　探讨人参皂苷Rbl(Ginsenoside Rb1,GSRb1)对大鼠局灶性脑缺血白质重塑的影响。 方法　大鼠随机分为假手术组、溶媒处理组和人参皂苷Rbl处理组,采用线栓法建立大鼠大脑中动脉缺血再灌注（middle cerebral artery occlusion/reperfusion, MCAO/R）损伤模型,用LFB染色观察大鼠胼胝体和内囊的髓鞘变化,用免疫组化染色法检测缺血侧胼胝体GFAP和APP的表达以评估星形胶质细胞和轴突的改变。 结果　缺血2 h再灌72 h后,溶媒处理组胼胝体和内囊有明显的髓鞘紊乱、脱失,胼胝体GFAP和APP表达显著增加。与溶媒处理组相比,GSRb1处理组髓鞘脱失有明显改善 (P<0. 01, P<0. 05)且胼胝体GFAP和APP表达显著减少(P<0. 05)。 结论　GSRb1可能促进大鼠局灶性脑缺血后脑白质重塑。     

慢性全脑低灌注大鼠侧脑室旁白质改变及基质金属蛋白酶-2和7的表达

目的观察慢性全脑低灌注大鼠侧脑室旁白质改变及基质金属蛋白酶-2和7(MMP-2和MMP-7)的表达并探讨其意义。方法 Wistar雄性大鼠60只,随机分为假手术组和模型组(20d组、40d组、60d组)共4组。模型组行双侧颈总动脉分期永久结扎术制备慢性全脑低灌注模型。透射电镜观察胼胝体和内囊超微结构变化;胶质纤维酸性蛋白(GFAP)免疫组织化学染色观察星形胶质细胞变化;免疫印迹法检测髓鞘碱性蛋白(MBP)含量变化;免疫组织化学染色和免疫印迹法观察和检测MMP-2和7表达变化。结果电镜观察可见模型20d组侧脑室旁白质有髓纤维髓鞘发生变形、板层结构疏松、崩溃等脱髓鞘改变,血管周围有明显水肿现象,而假手术组未见明显变化。各模型组见星形细胞胞体肥大、突触增粗、数量增多,随低灌注时间延长GFAP表达增多,而MBP减少,较假手术组差异均有明显统计学意义(P0.01)。各模型组MMP-2和MMP-7表达均较假手术组增多(P0.01或P0.001),MMP-2和MMP-7表达与侧脑室旁白质损伤呈明显正相关。结论大鼠慢性全脑低灌注引起持续性的侧脑室旁白质缺血性损伤,MMP-2和MMP-7表达上调可能参与白质损伤的进展。     

Gestational hypoxia induces white matter damage in neonatal rats: a new model of periventricular leukomalacia

In the premature infant, periventricular leukomalacia, usually related to hypoxicischemic white matter damage, is the main cause of neurological impairment. We hypothesized that protracted prenatal hypoxia might induce white matter damage during the perinatal period. Pregnant Sprague-Dawley rats were placed in a chamber supplied with hypoxic gas (10% O2-90% N2) from embryonic day 5 (E5) to E20. Neonatal rat brains were investigated by histology, immunocytochemistry, western blotting, in situ hybridization, DNA fragmentation analysis, and in vivo magnetic resonance imaging (MRI). Body weight of pups subjected to prenatal hypoxia was 10 to 30% lower from P0 to P14 than in controls. Specific white matter cysts were detected between P0 and P7 in pups subjected to prenatal hypoxia, in addition to abnormal extra-cellular matrix, increased lipid peroxidation, white matter cell death detected by TUNEL, and increased activated macrophage counts in white matter. Subsequently, gliotic scars and delayed myelination primarily involving immature oligodendrocytes were seen. In vivo MRI with T1, T2, and diffusion sequences disclosed similar findings immediately after birth, showing strong correlations with histological abnormalities. We speculate that protracted prenatal hypoxia in rat induces white matter damage occurring through local inflammatory response and oxidative stress linked to re-oxygenation during the perinatal period.     

胃癌中RUNX3、cyclin E和P21蛋白表达与患者生存的关系

目的：探讨胃癌RUNX3蛋白表达对细胞周期蛋白的影响及其与胃癌患者生存和生物学特性的关系。方法:应用免疫组化，分析RUNX3蛋白的表达；应用流式细胞术，分析cyclinE和P21蛋白表达；采用Kaplan-Meier限乘法计算生存率。结果:在56例胃癌中RUNX3蛋白、cyclinE和P21蛋白的阳性表达率分别为44.6%、64.3%和32.1%。胃癌细胞RUNX3蛋白表达与淋巴转移和远处转移有关(P<0.05)。胃癌细胞cyclinE的表达与浸润深度、淋巴转移和远处转移有关(P<0.05)。而胃癌细胞P21的表达与远处转移有关(P<0.05)。胃癌细胞中RUNX3和P21的表达之间呈明显正相关(r=0.57,P<0.05)，而与 cyclinE的表达之间无相关性(r=0.25,P>0.05)。用Kaplan-Meier生存曲线经Log-rank检验发现，RUNX3和cyclinE的阳性表达与生存相关(P<0.05)，P21的阳性表达与生存无关(P>0.05) 。结论：RUNX3蛋白可能通过影响P21蛋白的表达影响胃癌的发生发展；检测RUNX3和cyclinE的表达可作为反映胃癌临床病理学特点和预后的指标。     

Delayed white matter injury in a murine model of shaken baby syndrome

Shaken baby syndrome, a rotational acceleration injury, is most common between 3 and 6 months of age and causes death in about 10 to 40% of cases and permanent neurological abnormalities in survivors. We developed a mouse model of shaken baby syndrome to investigate the pathophysiological mechanisms underlying the brain damage. Eight-day-old mouse pups were shaken for 15 seconds on a rotating shaker. Animals were sacrificed at different ages after shaking and brains were processed for histology. In 31-day-old pups, mortality was 27%, and 75% of survivors had focal brain lesions consisting of hemorrhagic or cystic lesions of the periventricular white matter, corpus callosum, and brainstem and cerebellar white matter. Hemorrhagic lesions were evident from postnatal day 13, and cysts developed gradually between days 15 and 31. All shaken animals, with or without focal lesions, had thinning of the hemispheric white matter, which was significant on day 31 but not earlier. Fragmented DNA labeling revealed a significant increase in cell death in the periventricular white matter, on days 9 and 13. White matter damage was reduced by pre-treatment with the NMDA receptor antagonist MK-801. This study showed that shaking immature mice produced white matter injury mimicking several aspects of human shaken baby syndrome and provided evidence that excess release of glutamate plays a role in the pathophysiology of the lesions.     

The influence of DHEA pretreatment on prepulse inhibition and the HPA-axis stress response in rat offspring exposed prenatally to polyriboinosinic-polyribocytidylic-acid (PIC)

Periventricular leukomalacia (PVL) is the dominant form of brain injury in premature infants and no specific treatment is currently available. Neotrofin, a neurotrophin agonist, has been shown to provide neuroprotection in several in vivo and in vitro studies. The aim of this study was to investigate the neuroprotective effect of neotrofin treatment after endotoxin induced PVL in a rat model. Wistar rat pups were divided into four groups as: (1) control, (2) lipopolysaccharide (LPS)-administered group, (3) LPS-administered and prenatal maternal neotrofin-treated group and (4) LPS-administered and postnatal neotrofin-treated group. Intraperitoneal (i.p.) injection of lipopolysaccharide (LPS) was administered consecutively at the 18th and 19th embryonic days to establish endotoxin-induced PVL model. In the prenatal treatment group dams received an i.p. injection of neotrofin (60 mg/kg) following after the second LPS dose; and in the postnatal treatment group rat pups received i.p. injection of neotrofin (60 mg/kg) at birth. At P7, apoptosis and hypomyelination in periventricular white matter were evaluated by immunohistochemical assessments. The prenatal maternal neotrofin treatment significantly reduced the number of apoptotic cell death and greatly prevented LPS-stimulated loss of hypomyelinization. However, neotrofin treatment in the postnatal period was not as effective as intrauterine treatment. Given our results, neotrofin may be useful in reducing brain injury and possessing clinical relevance for the treatment of white matter injury in newborns.     

大鼠脊髓发育过程中神经干细胞的分化

目的:研究正常大鼠脊髓发育过程中神经干细胞的分化规律。方法:应用免疫荧光染色技术,检测Nestin、NeuN、MAP2、GFAP、CNPase阳性细胞在大鼠胚胎期及生后脊髓内的分布及变化情况。结果:胚胎发育早期,脊髓中央管、灰质、白质均可检测到Nestin阳性细胞,生后Nestin阳性细胞数量逐渐减少。大鼠脊髓神经元的发生呈现明显的背腹模式,孕14d(E14)脊髓内可检测到NeuN阳性细胞,E16 NeuN阳性细胞逐渐增多,腹侧NeuN阳性细胞核体积较大,分布较稀疏,背侧神经元细胞核体积较小,分布较密集。MAP2染色结果与NeuN一致。胶质细胞的分化、成熟在生后初期进行,P4可检测到GFAP及CNPase阳性细胞,主要分布于脊髓白质内,P30在脊髓灰质内可检测到GFAP阳性细胞,细胞分支较多且短。结论:正常大鼠脊髓发育中神经干细胞的分化呈现一定规律性,向神经元方向化较早且呈明显的背腹模式,胶质细胞的分化较晚。     

Apparent scarcity of glial fibrillary acidic protein expression in the brain of the pygmy shrew Sorex minutus as revealed by immunocytochemistry

We examined astroglial cells in the brain of the pygmy shrew Sorex minutus (Insectivora). For that purpose we labeled glial fibrillary acidic protein (GFAP) immunohistochemically in brain sections with a polyclonal antibody. Antigen retrieval experiments were performed to counteract formaldehyde fixation masking of GFAP epitopes. Our results showed remarkable paucity of GFAP-immunoreactive cells and fibers in the cerebral cortex and nuclei, as well as in the majority of the diencephalic and mesencephalic structures. In the forebrain, significant numbers of GFAP-containing astrocytes were found only in the ependyma and subventricular zones, superficial part of layer I of the cerebral cortex, and the majority of white matter structures. In the diencephalon, habenular nuclei were rich in GFAP-immunopositive astrocytes and labeled radial fibers were extended between median eminence and the third ventricle. A considerably higher density of labeled astrocytes was detected in the caudal brainstem and cerebellum. In contrast, in the mouse brain, immunoreactive astrocytes were present in large quantities in various structures. Staining of sections of the shrew brain against glutamine synthetase revealed abundance of immunofluorescent astrocytes in many areas, especially in the shrew cerebral cortex. It seems probable that in the shrew brain only a limited fraction of astroglia expresses GFAP, while other astroglial cells can be detected with different markers. It is possible that the rodent type of astroglial GFAP expression might not be common to insectivores and probably to some other mammalian orders.     

雌激素替代治疗对中年卵巢切除大鼠大脑白质、海马内髓鞘及Lingo-1蛋白的影响

目的检测经短期雌激素替代治疗(ERT)后中年卵巢切除大鼠大脑白质及海马内髓鞘相关指标及Lingo-1的表达,探讨雌激素对髓鞘作用的可能机制。方法 24只中年雌性SD大鼠行双侧卵巢切除术(OVX)后,随机分为安慰剂治疗组(OVX+Veh组)和雌激素替代治疗组(OVX+E组)。ERT 1个月后,Morris水迷宫检测大鼠空间学习和记忆能力;从各组大鼠随机选取10只,透射电子显微镜观察大脑白质及海马内髓鞘的超微结构;Western blot检测大脑白质及海马内髓磷脂碱性蛋白(MBP)及Lingo-1的含量;免疫组化方法检测Lingo-1在大脑白质及海马的分布。结果 OVX+E组大鼠在定位航行实验中的潜伏期显著短于OVX+Veh组大鼠(P0.05);OVX+Veh组大鼠大脑白质和海马存在显著的髓鞘结构变性;OVX+E组大鼠大脑白质和海马中MBP的含量均显著高于OVX+Veh组(P0.05),而OVX+E组大鼠大脑白质和海马中Lingo-1的含量及分布均显著低于OVX+Veh组(P0.05)。结论1个月的ERT对中年卵巢切除大鼠的认知功能及大脑白质和海马内的髓鞘具有明显的保护作用,这种保护作用可能与雌激素下调大脑白质和海马内Lingo-1蛋白的表达有关。     

急性脑梗死患者外周血淋巴细胞的早期活化与其黏附分子表达的关系研究

目的：探讨脑梗死患者外周血T淋巴细胞早期活化与黏附分子CD54和血小板P选择素（CD62P）、溶酶体颗粒糖蛋白63（CD63）的动态变化及临床意义。方法：用流式细胞仪检测32例脑梗死患者发病3d、7d外周血T淋巴细胞CD69和CD54及血小板CD62P、CD63的表达水平,并与35例健康者进行比较。结果：急性脑梗死（MS）患者发病72h内、7d外周血CD3^＋CD69^＋与CD3^＋CD54^＋及血小板CD62P与CD63表达阳性率均显著高于对照组（P〈0．01）,7d时各值虽较72h略降低,但差别无统计学意义（P〉0．05）;急性脑梗死患者发病72h内CD3^＋CD69^＋与CD3^＋CD54^＋、CD62P和CD63的表达无明显相关性（r值分别为-0．218、-0．117、-0．224,P〉0．05）;而CD54与CD62P、CD63的表达呈明显正相关（r=0．468,P〈0．01;r=0．397,P〈0．05）。结论：急性脑梗死后T淋巴细胞活化程度增强,其细胞表面CD54分子表达增高,同时血小板表面CD62P和CD63分子表达增加,活化的T淋巴细胞和血小板介导了白细胞与血小板及内皮细胞的黏附,加速了脑梗死的发生和发展,进一步加重了脑组织的损伤。     

短暂性缺氧对鼠脑神经源性分化因子表达的影响

目的观察短暂性缺氧后鼠脑神经源性分化因子(NeuroD)表达量的变化,初步探讨其在神经系统再生中的可能作用。方法"延迟剖宫产术"建立胎鼠宫内窘迫模型,通过RT-PCR检测窘迫不同时间后NeuroD mRNA表达量的变化,通过免疫荧光对NeuroD蛋白的表达进行定性分析。结果宫内窘迫5min,NeuroD mRNA表达量未见明显变化(P>0.05),窘迫10、15、20min后其表达量随窘迫时间的延长而不断增高。免疫荧光示在尾壳核区域NeuroD表达量明显增加。结论短暂性缺氧后NeuroD表达量增高,可能参与了神经系统的再生过程。