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首页> 美国卫生研究院文献>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诱导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 SC) 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 developmental stages of oligodendrocyte progenitors (O4 and O1) and by double-staining with terminal deoxynucleotidyl transferase-mediated digoxigenin–dUTP nick end-labeling (TUNEL) and O4 or O1. Administration of dexamethasone to neonatal rats reduced the expression of MBP in the white matter by P14. In addition, dexamethasone reduced the expression of O4-positive cells, presumably preoligodendrocytes, in the corpus callosum and induced degenerative changes, such as cytoplasmic condensation and fragmented, tortuous processes, 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天对新生大鼠施用了地塞米松（0.5 mg / kg SC）。免疫荧光染色和髓鞘碱性蛋白（Western blotting）检测髓鞘碱性蛋白（MBP） ）是在P14上执行的。通过对少突胶质祖细胞（O4和O1）不同发育阶段存在的表面标志物P5进行免疫荧光染色，并通过末端脱氧核苷酸转移酶介导的地高辛配基–dUTP尼克末端双染色，对与少突胶质祖细胞凋亡死亡相关的形态学变化进行了评估。标签（TUNEL）和O4或O1。地塞米松对新生大鼠的给药通过P14降低了白质中MBP的表达。此外，地塞米松减少了call体中O4阳性细胞（可能是前少突胶质细胞）的表达，并诱导了少突胶质细胞祖细胞的变性变化，例如细胞质凝缩和破碎的曲折过程，并增加了TUNEL阳性突触核的数量。少突胶质细胞祖细胞。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祖细胞凋亡的风险，随后导致髓鞘减少。

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