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首页> 外文期刊>The European Journal of Neuroscience >Restoration of impaired phosphorylation of cyclic AMP response element-binding protein (CREB) by EGb 761 and its constituents in Abeta-expressing neuroblastoma cells.
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Restoration of impaired phosphorylation of cyclic AMP response element-binding protein (CREB) by EGb 761 and its constituents in Abeta-expressing neuroblastoma cells.

机译：EGb 761及其组成成分在表达Abeta的神经母细胞瘤细胞中恢复环状AMP反应元件结合蛋白（CREB）磷酸化的受损。

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摘要

Cyclic AMP response element-binding protein (CREB) plays important roles in neuronal plasticity and amyloid beta-peptide (Abeta)-induced cognitive impairment in Alzheimer's disease (AD). Here we demonstrated that Ginkgo biloba extract, EGb 761, displayed the neuron protective effect by activating the CREB signaling pathway. Wild-type neuroblastoma cells cultured in a conditioned medium containing cell-secreted Alphabeta exhibited reduced levels of phosphorylated CREB (pCREB). Addition of EGb 761 (100 microg/mL) or an anti-oligomer-specific antibody (A-11) to the conditioned medium could restore pCREB level. In a neuroblastoma cell line expressing Alphabeta, treatment with EGb 761 increased levels of pCREB and brain-derived neurotrophic factor. Furthermore, CREB phosphorylation induced by EGb 761 was blocked by inhibitors of several upstream signaling pathways of CREB, including protein kinase C, ERK, ribosomal S6 kinase(RSK)90 and nitric oxide pathway. Moreover, these inhibitors differentially blocked the effects of individual components of EGb 761, ginkgolide C, quercetin and bilobalide, which suggest diverse effects of the EGb 761 individual components. Actions of individual EGb 761 components provide further insights into direct mechanisms underlying the effect of EGb 761 on enhancing the cognitive performance of patients with AD.
机译：环AMP反应元件结合蛋白（CREB）在神经元可塑性和淀粉样β肽（Abeta）诱导的阿尔茨海默病（AD）认知障碍中起重要作用。在这里，我们证明了银杏叶提取物EGb 761通过激活CREB信号通路显示了神经元保护作用。在含有细胞分泌的Alphabeta的条件培养基中培养的野生型神经母细胞瘤细胞显示出降低的磷酸化CREB（pCREB）水平。在条件培养基中加入EGb 761（100 microg / mL）或抗寡聚体特异性抗体（A-11）可以恢复pCREB水平。在表达Alphabeta的成神经细胞瘤细胞系中，用EGb 761进行治疗可增加pCREB和脑源性神经营养因子的水平。此外，EGB 761诱导的CREB磷酸化被CREB的几个上游信号通路的抑制剂所阻断，这些通路包括蛋白激酶C，ERK，核糖体S6激酶（RSK）90和一氧化氮通路。此外，这些抑制剂差异性地阻断了EGB 761，银杏内酯C，槲皮素和白果内酯的各个组分的作用，这提示了EGB 761各个组分的不同作用。各个EGb 761组件的作用可进一步深入了解EGb 761对增强AD患者认知能力的影响的直接机制。

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