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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Sodium butyrate suppresses interferon-gamma-, but not lipopolysaccharide-mediated induction of nitric oxide and tumor necrosis factor-alpha in microglia.
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Sodium butyrate suppresses interferon-gamma-, but not lipopolysaccharide-mediated induction of nitric oxide and tumor necrosis factor-alpha in microglia.

机译：丁酸钠抑制小胶质细胞中干扰素-γ，但不抑制脂多糖介导的一氧化氮和肿瘤坏死因子-α的诱导。

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摘要

In the present study, we demonstrate that sodium butyrate repressed IFN-gamma-induced expression of iNOS and TNF-alpha, but had little effect on LPS-induced expression in BV2 murine microglial cells. Sodium butyrate significantly inhibited NF-kappaB binding and NF-kappaB-mediated transcription induced by IFN-gamma, suggesting that the anti-inflammatory effect of sodium butyrate is mediated via specific inhibition of the NF-kappaB pathway. IFN-gamma is a major stimulator of innate and adaptive immune response. Thus, the specific down-regulation of IFN-gamma-induced microglial activation by sodium butyrate may provide potential therapeutic strategies for a variety of inflammatory diseases in the central nervous system.
机译：在本研究中，我们证明了丁酸钠抑制IFN-γ诱导的iNOS和TNF-α的表达，但对LPS诱导的BV2鼠小神经胶质细胞表达的影响很小。丁酸钠显着抑制IFN-γ诱导的NF-kappaB结合和NF-kappaB介导的转录，这表明丁酸钠的抗炎作用是通过特异性抑制NF-kappaB途径来介导的。 IFN-γ是先天性和适应性免疫反应的主要刺激物。因此，丁酸钠对IFN-γ诱导的小胶质细胞活化的特异性下调可能为中枢神经系统的多种炎性疾病提供潜在的治疗策略。

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