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首页> 外文期刊>Comparative Medicine >Administration of Dexamethasone to Neonatal Rats Induces Hypomyelination and Changes in the Morphology of Oligodendrocyte Precursors
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Administration of Dexamethasone to Neonatal Rats Induces Hypomyelination and Changes in the Morphology of Oligodendrocyte Precursors

机译：地塞米松对新生大鼠的给药可引起髓鞘过少和少突胶质细胞前体形态的变化

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To examine whether hypomyelination in neonatal rats might be related to apoptosis of oligodendrocyte progenitors, we administered dexamethasone (0.5 mg/kg SO to neonatal rats on postnatal (P) days 1 through 5. Immunofluorescent staining and Western blotting for myelin basic protein (MBP) were performed on P14. Morphologic changes associated with apoptotic death of oligodendrocyte progenitors were assessed by using immunofluorescent staining on P5 of surface markers present at different developmentalstages of oligodendrocyte progenitors (04 and Ol) and by double-staining with terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP nick end-labeling (TUNEL) and 04 or Ol. Administration of dexamethasone to neonatal rats reduced the expressionof MBP in the white matter by P14. In addition, dexamethasone reduced the expression of 04-positive cells, presumably preoligodendrocytes, in the corpus callosum and induced degenerative changes, such as cytoplasmic condensation and fragmented, tortuousprocesses, in oligodendrocyte progenitors, and increased the number of TUNEL-positive pyknotic nuclei of oligodendrocyte progenitors. These findings suggest that the dexamethasone-induced decreased expression of MBP in the cerebral hemispheres of the neonatal rats is due to apoptotic degeneration of oligodendrocyte progenitors. Administration of dexamethasone during the critical period of brain development may increase the risk of apoptosis in oligodendrocyte progenitors, subsequently resulting in hypomyelination.
机译：为了检查新生大鼠的低髓鞘形成是否可能与少突胶质细胞祖细胞的凋亡有关，我们在出生后（P）第1至5天给新生大鼠施用了地塞米松（0.5 mg / kg SO），进行了免疫荧光染色和髓鞘碱性蛋白（MBP）的Western印迹分析对少突胶质细胞祖细胞凋亡死亡相关的形态学变化进行了评估，方法是对少突胶质细胞祖细胞（04和Ol）不同发育阶段存在的表面标志物P5进行免疫荧光染色，并用末端脱氧核糖核苷酸转移酶介导的地高辛配基-双染色dUTP缺口末端标记（TUNEL）和04或Ol。向新生大鼠施用地塞米松可降低P14在白质中MBP的表达;此外，地塞米松还可降低call体中04阳性细胞（大概是少突胶质细胞）的表达。和诱导的退行性改变，例如细胞质凝缩和碎片化少突胶质细胞祖细胞中的曲折过程，并增加了少突胶质细胞祖细胞的TUNEL阳性缩聚核。这些发现表明，地塞米松诱导的新生大鼠脑半球中MBP表达的降低是由于少突胶质细胞祖细胞的凋亡性退化所致。在大脑发育的关键时期给予地塞米松可能会增加少突胶质细胞祖细胞凋亡的风险，随后导致髓鞘减少。

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