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1.
PURPOSE: To determine if posthypoxia treatment with erythropoietin (EPO) has protective effects against subsequent susceptibility to seizure related neuronal injury in rat pups subjected to acute hypoxia at P10. METHODS: Four groups of rats were manipulated at P10, as described below, then all received kainic acid (KA) (10 mg/kg i.p.) at P29: Hypoxia-NS-KA group (n = 11): subjected to acute hypoxia (down to 4% O2), and then immediately received saline i.p. Hypoxia-EPO-KA group (n = 10): subjected to acute hypoxia and then immediately received EPO (1,000 U/Kg i.p.). Normoxia-NS-KA group (n = 11): sham manipulated and injected with saline. Normoxia-EPO-KA group (n = 10): sham manipulated then immediately injected with EPO (1000 U/Kg i.p.). After receiving KA at P29, all rats were monitored using videotape techniques, and were sacrificed at P31. TUNEL and Hoechst stains to assess for apoptosis, and regular histology for hippocampal cell counts were performed. RESULTS: Administration of the single dose of erythropoietin directly after an acute hypoxic event at P10 resulted at P29 in increased latency to forelimb clonus seizures, reduced duration of these seizures, protection against hippocampal cell loss, and decreased hippocampal apoptosis in the Hypoxia-EPO-KA group as compared to the Hypoxia-NS-KA group. CONCLUSION: These data support the presence of favorable protective effects of erythropoietin against the long-term consequences of acute hypoxia in the developing brain and raise the possibility of its investigation as a potential neuroprotective agent after human neonatal hypoxic encephalopathy.  相似文献
2.
目的 研究瘦素对缺血缺氧性损伤的星形胶质细胞功能状态的影响. 方法 体外培养、纯化、鉴定SD乳鼠脑皮质星形胶质细胞,换用无血清低糖培养基在5%CO2+95%N2密闭盒中孵育90 min建立缺血缺氧损伤模型,应用RT-PCR方法 验证星形胶质细胞瘦素受体Ob-Ra和Ob-Rb的表达;采用比色法测定细胞上清液中乳酸脱氢酶(LDH)、丙二醛(MDA)的含量;通过免疫细胞化学方法 检测胶质纤维酸性蛋白质(GFAP)的表达水平. 结果缺血缺氧损伤后细胞出现严重坏死,与正常对照组比较,短型受体Ob-Ra表达无明显改变(3.87±0.13 vs 3.96±0.24,P>0.05),长型受体Ob-Rb表达水平明显降低(0.52±0.01 vs 1.32±0.01,P<0.05);细胞培养上清中LDH、MDA水平明显升高(709.68±47.16 vs 516.13±29.08、3.94±0.36 vs 1.81±0.21.P<0.05):细胞GFAP表达明显增强(0.122±0.016 vs 0.057±0.006,P<0.05).加入瘦素处理可维持细胞形态基本完整,与缺血缺氧损伤组比较,LDH、MDA水平明显降低,其中MDA两组间比较差异有统计学意义(3.19±0.25vvs 3.94±0.36,P<0.05),GFAP表达也明显增强(0.109±0.008 vs 0.057±0.006,P<0.05). 结论 瘦素能够明显提高星形胶质细胞对缺血缺氧损伤的耐受性,具有神经保护作用.  相似文献
3.
BACKGROUND: Angelica sinensis is a widely used herb in Chinese traditional medicine. It has been shown to improve hypoxia in embryonic rats and reduce nestin expression in neural stem cells, resulting in proliferation of neural stem cells.
OBJECTIVE: To study the protective effect of Angelica on neural stem cell proliferation in neonatal rats after intrauterine hypoxia.
DESIGN, TIME AND SETTING: The randomized, controlled, experiment was performed at the Department of Histology and Embryology, Luzhou Medical College, China from July 2007 to January 2008.
MATERIALS: Because gestational days 14-15 are a key stage in rat nervous system development, 21 healthy, pregnant Sprague Dawley rats (14 days after conception) were used for this study. Nestin monoclonal primary antibody was obtained from Chemicon, USA. Angelica parenteral solution (250 g/L) was obtained from Pharmaceutical Preparation Section, Second Affiliated Hospital of Wuhan University, China.
METHODS: Rats were randomly divided into a control group (n = 5), a hypoxia group (n = 8), and an Angelica group (n = 8). Saline (8 mL/kg) was injected into the caudal vein of rats in the hypoxia group once a day for seven consecutive days. Intrauterine hypotonic hypoxia was induced using 13% O2 for two hours per day on three consecutive days. Rats in the Angelica group received injections of Angelica parenteral solution (250 g/L); all other protocols were the same as the hypoxia group. The control group procedures were identical to the hypoxia group, but under normal, non-hypoxic conditions. After birth, brain tissues were immediately obtained from neonatal rats and prepared for nestin immunohistochemistry.
MAIN OUTCOME MEASURES: Nestin-positive cells in hippocampal CA3 area of neonatal rats in each group were quantified using image analysis to detect signal absorbance.
RESULTS: The number of nestin-positive cells increased in the hippocampal CA3 area of neonatal rats in the hypoxia group. The number of nestin-pos  相似文献
4.
Systemic Effects of Generalized Convulsive Status Epilepticus   总被引:2,自引:2,他引:3  
Nancy Y. Walton 《Epilepsia》1993,34(S1):S54-S58
Summary: Generalized convulsive status- epilepticus (GCSE) is accompanied by a marked increase in plasma catecholamines. This produces a number of changes in general systemic physiology including hypertension, tachycardia, cardiac arrhythmias, hyperglycemia, acidosis, and hyperpyrexia. If SE is stopped quickly, these changes are self-correcting and do not produce an increased risk of neuropathology. However, if seizures continue, many of the early physiologic changes reverse, and late status epilepticus is marked by hypotension, hypoglycemia, pulmonary edema and a continued acidosis and elevation of body temperature. Prevention of serious hypoglycemia, maintenance of adequate systemic blood pressure to provide adequate cerebral perfusion, and normalizing the body temperature will minimize or prevent neuropathologic sequelae to SE of extended duration.  相似文献
5.
巴曲酶对海马脑片缺氧损伤的保护作用   总被引:2,自引:2,他引:14  
本实验采用离体大鼠海马脑片缺氧模型,观察巴曲酶对缺氧后海马脑片CA1区诱发突触电位的影响。结果可见:用三种浓度巴曲酶孵育的海马脑片缺氧后PV消失时间均明显延迟,但对PS的消失时间无明显影响。提示:巴曲酶对海马神经元缺氧损伤具有一定保护作用。  相似文献
6.
目的:观察氦甲酰化促红细胞生成素衍生物(CEPO)对低氧所致小鼠海马损伤的保护作用。方法:成年雄性C57/B6小鼠置低氧(8%O2)分别处理0,5、1.5、3和6h,记录各组小鼠复氧后连续6及30d的Y迷宫训练错误反应次数。用免疫组化检测海马神经元核蛋白(NeuN)。在此基础上,将经Y迷宫训练筛选的小鼠低氧处理6h,并分为3组:CEPO组、促红细胞生成素(EPO)组和生理盐水组,隔日1次分别腹腔注射CEPO、EPO和生理盐水,共15次。第10和30天对小鼠进行Y迷宫测试,记录错误反应次数。用NeuN免疫组化检测给予药物干预2次(72h)后各组小鼠海马神经元的脱失状况。结果:①低氧处理的小鼠学习能力明显下降,以低氧3h组和6h组尤为明显;第30天Y迷宫测试时,低氧6h组的错误反应次数最高;NeuN免疫染色显示低氧后复氧3d的各组小鼠海马各亚区神经元均有明显脱失,以低氧6h组最为明显。②第10和30天Y迷宫测试显示,低氧小鼠经CEPO或EPO干预后Y迷宫的错误反应次数明显低于生理盐水处理的小鼠;NeuN免疫染色显示低氧小鼠给予CEPO或EPO处理后海马神经元脱失明显少于生理盐水处理的小鼠。结论:低氧处理6h的小鼠学习和记忆能力明显降低,海马神经元损伤严重。CEPO具有与EPO相似的减轻低氧所致学习和记忆损伤、减少海马神经元脱失的作用。  相似文献
7.
Neurotoxicological effects of 3-nitropropionic acid on the neonatal rat   总被引:2,自引:0,他引:2  
Wang T  Zhang L  Jiang L  He N 《Neurotoxicology》2008,29(6):1023-1029
An increasing amount of data provides support for the hypothesis that periventricular leukomalacia (PVL) results from pre- or perinatal hypoxia occurring and is a major cause of cerebral palsy. In this work, anoxic and hypoxic–ischemic brain injuries were observed by us, after injection of neurotoxin 3-nitropropionic acid (3-NP) in a neonatal rat model on postnatal day 5 (P5). 3-NP-induced brain injury was examined in fixed brain sections at 24 h (P6), 48 h (P7), 72 h (P8), and 9 days (P14) after 3-NP injection, respectively. Injection with 3-NP results in pathological injuries including white matter lesions, cerebral cortex destruction, callose thinness, and cerebral ventricle expansion. Numbers of immature oligodendrocytes turned to less in the model of 3-NP. Furthermore myeline basic protein expression became significantly lower after 3-NP was injected. Pathological changes after injection of 3-NP appeared also significantly among rats of postnatal day 5. The effect of the 3-NP neurotoxicity paradigm was evaluated in this study to further investigate the underlying pathology associated with PVL, which may yield a potential desirable model for clinic experiments.  相似文献
8.
Neonatal maternal separation (NMS) alters respiratory control development. Adult male rats previously subjected to NMS show a hypoxic ventilatory response 25% greater than controls. During hypoxia, γ-aminobutyric acid (GABA) release within the nucleus tractus solitarius (NTS) modulates the magnitude of the ventilatory response. Because development of GABAergic receptors is sensitive to NMS, we tested the hypothesis that in adults, a change in responsiveness to GABA within the NTS contributes to NMS-related enhancement of the inspiratory (phrenic) response to hypoxia. Pups subjected to NMS were placed in an incubator for 3 h/day for 10 consecutive days [postnatal days 3 to 12]. Controls were undisturbed. Adult (8–10 weeks old) rats were anaesthetized (urethane; 1.6 g/kg), paralysed and artificially ventilated to record phrenic activity. Rats either received a 50-nL microinjection of GABA (5 µ m ) or phosphate-buffered saline (sham) within the caudal NTS, or no injection prior to being exposed to hypoxia (FiO2 = 0.12; 5 min). NMS enhanced both the frequency and amplitude components of the phrenic response to hypoxia vs controls. GABA microinjection attenuated the phrenic responses in NMS rats only. This result is supported by ligand binding autoradiography results showing that the number of GABAA receptors within the NTS was 69% greater in NMS vs controls. Despite this increase, the phrenic response to hypoxia of NMS rats is larger than controls, suggesting that the higher responsiveness to GABA microinjection within the NTS is part of a mechanism that aims to compensate for: (i) a deficient GABAergic modulation; (ii) enhancement of excitatory inputs converging onto this structure; or (iii) both.  相似文献
9.
10.
Fu X  Li Q  Feng Z  Mu D 《Glia》2007,55(9):935-941
Aquaporin-4 (AQP4), a water channel protein, is abundantly expressed in astrocytes and plays a key role in the development of brain edema. However, it is not clear whether AQP4 contributes to astrocytic swelling in hypoxia-ischemia (HI). To investigate the roles of AQP4 in astrocytic swelling during HI and reoxygenation, we measured AQP4 expression and astrocytic cellular volume in cultured rat astrocytes following HI and reoxygenation. RNA interference was used to knockdown AQP4 expression (AQP4(-/-)). Real-time polymerase chain reaction and Western blot analysis were used to detect the inhibitory efficiency of AQP4. We found that the maximal inhibition of AQP4 mRNA and protein in astrocytes after AQP4 siRNA transfection (AQP4(-/-)) was approximately 77 and 85%, respectively, compared to wild-type AQP4 (AQP4(+/+)) expression. Cellular volume in both AQP4(-/-) and AQP4(+/+) astrocytes was significantly increased during HI compared to cells cultured in normoxia (P<0.05). However, cellular volume during HI in AQP4(-/-) astrocytes was significantly less than that in AQP4(+/+) astrocytes (P<0.05). After reoxygenation, the cellular volume gradually decreased to control levels at 7 days in AQP4(-/-) but at 5 days in AQP4(+/+) astrocytes. The different roles of AQP4 during HI and reoxygenation suggest that AQP4 knockdown may protect against water influx in the formation of astrocyte swelling during HI, and may also delay water clearance in the resolution of astrocyte swelling during reoxygenation. In conclusion, AQP4 mediates bidirectional transport of water across astrocytes during HI and reoxygenation. AQP4 manipulation may serve as a novel therapeutic strategy during different periods of hypoxic-ischemic brain edema in neonates.  相似文献
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