Treatment of Neurodegenerative disease with recombinent cells

1)检测重组脑源性神经营养因子(BDNF)和神经生长因子(NGF)对培养的大鼠皮质神经元的影响。皮质神经元短暂暴露于谷氨酸，然后与无谷氨酸的培养液孵育，与对照组相比，细胞存活率降低了60%-70%。在含有谷氨酸的大鼠皮质培养物中同时加入重组BDNF和NGF，并不影响细胞存活率的降低。然而，用重组BDNF NGF处理大鼠皮质细胞24小时后，谷氨酸诱导的神经元损伤明显减轻。这些结果表明BDNF NGF对谷氨酸诱导的神经毒性有保护作用。2)我们观察了大鼠短暂性前脑缺血后BDNF和NGF基因表达的变化以及BDNF和NGF对神经元死亡的影响。结果提示，短暂性脑缺血后，海马区和脑…区脑源性神经营养因子和神经生长因子基因表达均增强。3)在L-甲基-4-苯基-1，2，3，6-四氢吡啶诱导的猴帕金森病模型上，观察了鞘内注射脑源性神经营养因子的影响。BDNF组动物在第一周无症状，第二周表现为轻度帕金森综合症，而非BDNF组动物在第一周出现典型的帕金森综合征，第二周恶化。黑质的组织学损害与临床特征密切相关。重度帕金森病动物(非脑源性神经营养因子组)黑质神经细胞严重丢失，而脑源性神经营养因子组黑质神经细胞损伤明显减轻。提示BDNFHAS可能对MPTP诱导的帕金森病猴的神经综合征和黑质组织学损伤有预防作用。较少

1) The effect of recombinant brain-derived neurotrophic factor (BDNF) nerve growth factor (NGF) on cultured rat cortical neurons was examined. Brief exposure of cortical neurons to glutamate followed by incubation with glutamate-free medium reduced cell viability by 60-70% when compared with the control value. Simultaneous addition of recombinant BDNF NGF to rat cortical cultures with glutamate did not effect this reduction of cell viability. However, 24h pretreatment of rat cortical cultures with recombinant BDNF NGF resulted in a significant reduction of glutamate-induced neuronal damage. These findings suggest that BDNF NGF can protect cortical neurons against glutamate-induced neurotoxicity.2) We investigated alterations in BDNF and NGF gene expression and the effect of BDNF and NGF on neuronal death after transient forebrain ischemia in the rat brain. The results suggested that BDNF and NGF gene expression was enhanced by transient ischemia both in the hippocampus and the cerebral … More cortex and that BDNF or NGF,at a sufficient dose, has a preventive effect on the delayd hippocampal neuronal death observed after transient forebrain ischemia.3) The effects of the intrathecal infusion of brain-derived neurotrophic factor (BDNF) were examined in a l-methy1-4-phenyl-1,2,3,6-tetrahydropiridine (MPTP) -induced parkinsonian model in monkeys. The BDNF-treated animals remained asymptomatic during the first week and showed mild parkinsonism during the second week, whereas the non-BDNF group showed typical parkinsonian syndrome during the first week, deteriorating in the second week. Histological damage in the substantia nigra correlated well with the clinical features. Severe neuronal cell loss in the substantia nigra was observed in animals with severe Parkinsonism (those in the non-BDNF group), while the neuronal cell damage in the substantia nigra was significantly less in the BDNF group. These findings suggest that BDNF has may have a preventive effect on the neurological syndrome and the histological damage of the substantia nigra in MPTP-induced Parkinsonism in monkeys. Less