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大鼠过氧化物酶体β-氧化的实验性抑制:对脑髓鞘形成的影响

Experimental inhibition of peroxisomal beta-oxidation in rats: influence on brain myelination.

作者信息

Van den Branden C, Leeman J, Dacremont G, Collumbien R, Roels F

机构信息

Laboratorium voor Menselijke Anatomie, Vrije Universiteit Brussel, Belgium.

出版信息

Glia. 1990;3(6):458-63. doi: 10.1002/glia.440030604.

Abstract

Oral administration of thioridazine, an inhibitor of peroxisomal beta-oxidation, to normal rats from weaning till day 60 causes a small increase of the very long chain fatty acid C26 in brain lipids. Myelination in the brain is decreased. In the genu of the corpus callosum the ratio of non-myelinated/myelinated axons is increased. In the commissura anterior the myelin sheaths of the axons are significantly thinner in treated than in control animals. Undernourishment caused by the drug is minimal in this experiment. Area and total DNA of glial nuclei are unaltered in both the genu and the commissura anterior of treated rats. The distribution of chromatin (texture), however, shows small differences in the corpus callosum.

摘要

从断奶到60日龄对正常大鼠口服硫利达嗪(一种过氧化物酶体β氧化抑制剂),会导致脑脂质中极长链脂肪酸C26略有增加。脑内髓鞘形成减少。在胼胝体膝部,无髓鞘/有髓鞘轴突的比例增加。在胼胝体前连合处,与对照动物相比,经处理动物轴突的髓鞘明显更薄。在本实验中,药物引起的营养不良极小。经处理大鼠的胼胝体膝部和胼胝体前连合处的神经胶质细胞核面积和总DNA均未改变。然而,染色质的分布(质地)在胼胝体中显示出微小差异。

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