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首页> 外文期刊>Journal of neuroendocrinology >Corticosteroids impair remyelination in the corpus callosum of cuprizone-treated mice.
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Corticosteroids impair remyelination in the corpus callosum of cuprizone-treated mice.

机译：皮质类固醇会损害铜酮治疗小鼠的call体的髓鞘再生。

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Corticosteroids (CS) are effective in the treatment of many brain disorders, such as multiple sclerosis (MS) or traumatic brain injury. This has been scrutinised in different experimental animal models. However, neither the mechanisms, nor the site of CS action are fully understood. Short-term high-dose CS treatment improves MS symptoms and severity of clinical disability during an acute inflammatory exacerbation of disease. In the present study, we analysed the influence of CS on the expression of cellular and molecular markers of spontaneous endogenous remyelination in the toxic non-immune cuprizone animal model at early (9 days) and intermediate (21 days) remyelination, as well as steroidal effects in primary astrocytes and oligodendrocyte progenitor cultures. Dexamethasone (Dex) and methylprednisolone (MP) induced a higher expression of the differentiation markers myelin basic protein and proteolipid protein (PLP) in cultured oligodendrocyte progenitor cells (OPC). CS exposure of primary cultured astrocytes resulted in a greater expression of those genes involved in OPC proliferation [fibroblast growth factor 2 (FGF2) and platelet-derived growth factor (PDGF)-alphaalpha] and a reduced expression of the pro-maturation factor insulin-like growth factor 1. Pro-maturating effects of CS were completely blocked by FGF2 and PDGF-alphaalpha co-application in OPC cultures. MP treatment in vivo resulted in a reduced recovery of PLP-staining intensity, whereas the re-population of the demyelinated corpus callosum with adenomatous polyposis coli-expressing oligodendrocytes was not affected. The numbers of brain intrinsic inflammatory cells, microglia and astrocytes during remyelination were similar in placebo and MP-treated animals. Our findings suggest that treatment with CS might have, in addition to the well-known benefical effects on inflammatory processes, a negative influence on remyelination.
机译：皮质类固醇（CS）可有效治疗多种脑部疾病，例如多发性硬化症（MS）或颅脑外伤。已经在不同的实验动物模型中对此进行了仔细研究。但是，对CS的机制和作用部位都没有完全了解。短期大剂量CS治疗可改善MS症状和急性炎症加重期间的临床残疾严重程度。在本研究中，我们分析了CS对有毒非免疫铜酮动物模型中早期（9天）和中期（21天）髓鞘再生以及甾体类固醇的自发性内源性髓鞘再生的细胞和分子标记表达的影响。在原代星形胶质细胞和少突胶质祖细胞培养中的作用。地塞米松（Dex）和甲基泼尼松龙（MP）在培养的少突胶质祖细胞（OPC）中诱导分化标志物髓磷脂碱性蛋白和蛋白脂蛋白（PLP）的更高表达。 CS暴露于原代培养的星形胶质细胞会导致参与OPC增殖的那些基因[成纤维细胞生长因子2（FGF2）和血小板衍生的生长因子（PDGF）-α]的表达更高，促成熟因子胰岛素-像生长因子1。CS的促成熟作用完全被OPC培养物中的FGF2和PDGF-alphaalpha共同阻断。体内的MP处理导致PLP染色强度的恢复降低，而脱髓鞘的call体和表达腺瘤性息肉的少突胶质细胞的重新繁殖没有受到影响。在安慰剂和MP处理的动物中，髓鞘再生期间大脑内在的炎症细胞，小胶质细胞和星形胶质细胞的数量相似。我们的发现表明，除了众所周知的对炎症过程的有益作用外，CS治疗可能还会对髓鞘再生产生负面影响。

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