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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >An in vitro model for the study of microglia-induced neurodegeneration: involvement of nitric oxide and tumor necrosis factor-alpha.
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An in vitro model for the study of microglia-induced neurodegeneration: involvement of nitric oxide and tumor necrosis factor-alpha.

机译：研究小胶质细胞引起的神经变性的体外模型：一氧化氮和肿瘤坏死因子-α的参与。

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The precise function of activated microglia and their secretory products remains controversial. In order to assess the role of microglial secretion products, we established an in vitro model of an inflammatory reaction in the brain by co-culturing microglial and neuronal cell lines. Upon stimulation with interferon-gamma and lipopolysaccharides, the microglial cells adopted an activated phenotype and secreted tumor necrosis factor-alpha (TNF-alpha), prostaglandin E(2) and nitric oxide (NO). Neuronal degeneration was quantified by measuring the concentrations of microtubule associated protein tau and neuron specific enolase, which are also used as diagnostic tool in Alzheimer's disease, in supernatants. In activated contact co-cultures, the levels of these neuronal markers were significantly raised compared to non-activated co-cultures. NO-synthase inhibitors significantly diminished the rise of tau in activated co-cultures, while indomethacin, superoxide dismutase, or a neutralizing TNF-alpha antibody did not. When a chemical NO-donor or TNF-alpha were added to pure neuronal cultures, cell viability was significantly reduced. TNF-alpha increased neuronal sensitivity towards NO. There were indications that a part of the cells died by apoptosis. This model demonstrates a neurotoxic role for NO in microglia-induced neurodegeneration and provides a valuable in vitro tool for the study of microglia-neuron interactions during inflammation in the brain.
机译：活化的小胶质细胞及其分泌产物的确切功能仍存在争议。为了评估小胶质细胞分泌产物的作用，我们通过共同培养小胶质细胞和神经元细胞系，建立了大脑炎症反应的体外模型。干扰素-γ和脂多糖刺激后，小胶质细胞采用激活的表型，并分泌肿瘤坏死因子-α（TNF-alpha），前列腺素E（2）和一氧化氮（NO）。通过测量上清液中微管相关蛋白tau和神经元特异性烯醇化酶的浓度来量化神经元变性，tau和神经元特异性烯醇化酶也可用作阿尔茨海默氏病的诊断工具。在活化的接触共培养物中，与未活化的共培养物相比，这些神经元标记物的水平显着升高。 NO-合酶抑制剂可显着减少活化共培养物中tau的升高，而吲哚美辛，超氧化物歧化酶或中和的TNF-α抗体则不能。当将化学NO供体或TNF-α添加到纯神经元培养物中时，细胞活力显着降低。 TNF-α增加了对NO的神经元敏感性。有迹象表明部分细胞因凋亡而死亡。该模型证明了NO在小胶质细胞诱导的神经变性中的神经毒性作用，并为研究脑部炎症期间小胶质细胞与神经元的相互作用提供了有价值的体外工具。

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