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首页> 外文期刊>The European Journal of Neuroscience >Astrocytic factors protect neuronal integrity and reduce microglial activation in an in vitro model of N-methyl-D-aspartate-induced excitotoxic injury in organotypic hippocampal slice cultures.
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Astrocytic factors protect neuronal integrity and reduce microglial activation in an in vitro model of N-methyl-D-aspartate-induced excitotoxic injury in organotypic hippocampal slice cultures.

机译：在器官型海马切片培养物中，N-甲基-D-天冬氨酸诱导的兴奋性毒性损伤的体外模型中，星形胶质细胞因子保护神经元完整性并减少小胶质细胞活化。

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Acute CNS lesions lead to neuronal injury and a parallel glial activation that is accompanied by the release of neurotoxic substances. The extent of the original neuronal damage can therefore be potentiated in a process called secondary damage. As astrocytes are known to secrete immunomodulatory and neuroprotective substances, we investigated whether astrocytic factors can attenuate the amount of neuronal injury as well as the degree of microglial activation in a model of excitotoxic neurodegeneration. Treatment of organotypic hippocampal slice cultures with N-methyl-D-aspartate (NMDA) resulted in a reproducible loss of viable granule cells, partial destruction of the regular hippocampal cytoarchitecture and a concomitant accumulation of amoeboid microglial cells at sites of neuronal damage. Astrocyte-conditioned media reduced the amount of NMDA-induced neuronal injury by 45.3%, diminished the degree of microglial activation and resulted in an improved preservation of the hippocampal cytoarchitecture. Transforming growth factor (TGF)-beta failed to act as a neuroprotectant and even enhanced the amount of neuronal injury by 52.5%. Direct effects of astrocytic factors on isolated microglial cells consisted of increased microglial ramification and down-regulated expression of intercellular adhesion molecule-1, whereas incubation with TGF-beta had no such effects. In summary, our findings show that hitherto unidentified astrocyte-derived factors that are probably not identical with TGF-beta can substantially enhance neuronal survival, either by eliciting direct neuroprotective effects or by modulating the microglial response to neuronal injury.
机译：急性中枢神经系统病变导致神经元损伤和神经胶质细胞平行活化，并伴有神经毒性物质的释放。因此，可以在称为继发性损伤的过程中增强原始神经元损伤的程度。由于已知星形胶质细胞会分泌免疫调节和神经保护物质，因此我们研究了星形胶质细胞因子是否可以在兴奋性毒性神经变性模型中减轻神经元损伤的程度以及小胶质细胞活化的程度。用N-甲基-D-天门冬氨酸（NMDA）处理器官型海马切片培养物导致可再生的存活颗粒细胞丢失，部分海马常规细胞结构破坏以及在神经元损伤部位伴随形成的类小胶质细胞积聚。星形胶质细胞条件培养基将NMDA诱导的神经元损伤的量减少45.3％，减少了小胶质细胞活化的程度，并改善了海马细胞结构的保存。转化生长因子（TGF）-β不能充当神经保护剂，甚至使神经元损伤的程度增加了52.5％。星形胶质细胞因子对分离的小胶质细胞的直接作用包括增加的小胶质细胞分枝和下调细胞间粘附分子-1的表达，而与TGF-β一起孵育则没有这种作用。总而言之，我们的发现表明，迄今未发现的星形胶质细胞衍生因子可能与TGF-β不同，可以通过引起直接的神经保护作用或通过调节对神经元损伤的小胶质细胞反应来实质上提高神经元的存活率。

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