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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 >Molecular mechanisms of glucocorticoid resistance in splenocytes of socially stressed male mice.
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Molecular mechanisms of glucocorticoid resistance in splenocytes of socially stressed male mice.

机译：社会应激雄性小鼠脾细胞中糖皮质激素抵抗的分子机制。

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摘要

Splenocytes from socially stressed male mice display functional glucocorticoid (GC) resistance, viz., the antiproliferative effects of GC on lipopolysaccharide (LPS)-stimulated splenocytes is absent. In this study, we investigated changes in the structure and function of the glucocorticoid receptor (GR) in socially stressed animals. Changes of GR at both DNA and RNA levels were excluded. Reduced GR function was restricted to macrophages (CD11b(+)) in association with impaired nuclear translocation of GR after GC stimulation. Consequently, GC failed to block the activation of NF-kappa B in these cells. Thus, impaired nuclear translocation of GR and the lack of transcriptional suppression of NF-kappa B by GC were identified as the molecular mechanisms responsible for the observed GC resistance in spleens of socially stressed mice.
机译：受社会压力的雄性小鼠的脾细胞表现出功能性糖皮质激素（GC）抵抗力，即不存在GC对脂多糖（LPS）刺激的脾细胞的抗增殖作用。在这项研究中，我们调查了社会应激动物中糖皮质激素受体（GR）的结构和功能的变化。排除了在DNA和RNA水平上GR的变化。 GR功能降低仅限于巨噬细胞（CD11b（+））与GC刺激后GR核易位受损相关。因此，GC无法阻止这些细胞中NF-κB的活化。因此，GC的GR核易位障碍和NF-κB转录抑制的缺乏被认为是引起社会压力的小鼠脾脏中观察到的GC抗性的分子机制。

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