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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 >Microglial activation is inhibited by corticosterone in dopaminergic neurodegeneration.
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Microglial activation is inhibited by corticosterone in dopaminergic neurodegeneration.

机译：皮质酮在多巴胺能神经变性中抑制小胶质细胞活化。

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The present study compared 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced microglial activation in 3 different groups, sham-operated (SHM) mice, adrenalectomized mice (ADX), and ADX mice administered with corticosterone (ADX + CORT), to investigate the roles of glucocorticoids on microglial activation and dopaminergic neurodegeneration. Acute MPTP treatment induced moderate tyrosine hydroxylase (TH)-immunoreactive neuronal loss in the substantia nigra (SN) of SHM mice; this neuronal loss was significantly enhanced in ADX mice, but eventually recovered following the administration of corticosterone. Consistent with neuronal findings, acute MPTP treatment induced microglial activation in the SN from 1-3 days post injection in SHM mice. Interestingly, microglial activation was further enhanced and occasionally showed a phagocytic morphology in ADX mice that showed no circulating corticosterone. Furthermore, the activated microglia was significantly suppressed by the administration of corticosterone to ADX mice. Moreover, a confocal microscopic study demonstrated that the expression of inducible nitric oxide synthase protein, exclusively colocalized with activated microglia in the SN in ADX mice, was substantially decreased by the administration of corticosterone. Thus, the present study, using in-vivo adrenalectomy for a dopaminergic neurodegeneration model, successfully demonstrated the neuroprotective effects of corticosterone by microglial inhibition.
机译：本研究比较了3个不同组（假手术（SHM）小鼠，肾上腺切除小鼠（ADX）和ADX小鼠）中的1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的小胶质细胞活化与皮质酮（ADX + CORT）一起使用，以研究糖皮质激素在小胶质细胞激活和多巴胺能神经退行性变中的作用。急性MPTP处理可引起SHM小鼠黑质（SN）中度酪氨酸羟化酶（TH）-免疫反应性神经元丢失;这种神经元损失在ADX小鼠中明显增强，但在服用皮质酮后最终得以恢复。与神经元发现一致，从SHM小鼠注射后的1-3天起，急性MPTP处理可诱导SN中的小胶质细胞活化。有趣的是，小胶质细胞的激活进一步增强，并且在ADX小鼠中偶尔显示出吞噬细胞形态，没有显示循环皮质酮。此外，通过向ADX小鼠施用皮质酮显着抑制了活化的小胶质细胞。此外，共聚焦显微镜研究表明，在皮下注射皮质酮，可诱导的一氧化氮合酶蛋白（仅与活化的小胶质细胞共定位在SN的SN中）的表达大大降低。因此，本研究使用体内肾上腺切除术治疗多巴胺能神经退行性模型，成功地通过小胶质细胞抑制作用证明了皮质酮的神经保护作用。

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