Department of Biological Sciences, Geauga campus, Kent State University, Burton, Ohio, United States of America.
Department of Chemistry and Biology, University of Akron, Akron, Ohio, United States of America.
PLoS One. 2018 Aug 27;13(8):e0203057. doi: 10.1371/journal.pone.0203057. eCollection 2018.
Multiple sclerosis (MS) is a devastating neurological disease, which is characterized by multifocal demyelinating lesions in the central nervous system. The most abundant myelin lipids are galactosylceramides and their sulfated form, sulfatides, which together account for about 27% of the total dry weight of myelin. In this study we investigated the role of vitamin K in remyelination, by using an animal model for MS, the cuprizone model. Demyelination was induced in C57Bl6/J mice, by feeding them a special diet containing 0.3% cuprizone (w/w) for 6 weeks. After 6 weeks, cuprizone was removed from the diet and mice were allowed to remyelinate for either 1 or 3 weeks, in the absence or presence of vitamin K (i.p. phylloquinone, 2mg, three times per week). Vitamin K enhanced the production of total brain sulfatides, after both 1 week and 3 weeks of remyelination (n = 5, P-values were <0.0001), when compared with the control group. To determine whether or not there is a synergistic effect between vitamins K and D for the production of brain sulfatides, we employed a similar experiment as above. Vitamin K also increased the production of individual brain sulfatides, including d18:1/18:0, d18:1/20:0, d18:1/24:0, and d18:1/24:1 after 3 weeks of remyelination, when compared to the control group. In addition, vitamin D enhanced the production of total brain sulfatides, as well as d18:1/18:0, d18:1/24:0, and d18:1/24:1 sulfatides after 3 weeks of remyelination, but no synergistic effect between vitamins K and D for the production of total brain sulfatides was observed.
多发性硬化症(MS)是一种破坏性的神经疾病,其特征是中枢神经系统中有多处脱髓鞘病变。最丰富的髓鞘脂质是半乳糖脑苷脂及其硫酸化形式硫酸脑苷脂,它们共占髓鞘干重的约 27%。在这项研究中,我们通过使用 MS 的动物模型——铜缺乏模型,研究了维生素 K 在髓鞘再生中的作用。通过用含有 0.3%铜(w/w)的特殊饮食喂养 C57Bl6/J 小鼠 6 周来诱导脱髓鞘。6 周后,从饮食中去除铜,并允许小鼠在缺乏或存在维生素 K(腹腔注射叶绿醌,2mg,每周 3 次)的情况下再髓鞘化 1 或 3 周。与对照组相比,维生素 K 增强了总脑硫酸脑苷脂的产生,无论是在再髓鞘化 1 周还是 3 周后(n=5,P 值均<0.0001)。为了确定维生素 K 和 D 是否对脑硫酸脑苷脂的产生有协同作用,我们进行了类似的实验。与对照组相比,维生素 K 还增加了 18:1/18:0、18:1/20:0、18:1/24:0 和 18:1/24:1 等个别脑硫酸脑苷脂的产生,这是在再髓鞘化 3 周后。此外,维生素 D 增强了总脑硫酸脑苷脂以及 18:1/18:0、18:1/24:0 和 18:1/24:1 硫酸脑苷脂的产生,但维生素 K 和 D 对总脑硫酸脑苷脂的产生没有协同作用。