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首页> 外文期刊>Journal of Nutritional Science and Vitaminology >Mechanism in inhibitory effects of vitamin K2 on osteoclastic bone resorption: in vivo study in osteopetrotic (op/op) mice.
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Mechanism in inhibitory effects of vitamin K2 on osteoclastic bone resorption: in vivo study in osteopetrotic (op/op) mice.

机译：维生素K2对破骨细胞骨吸收的抑制作用机理：在骨石化（op / op）小鼠中的体内研究。

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Osteoclast deficiency in op/op mice was cured by a single injection of 5 micrograms recombinant human macrophage colony-stimulating factor (M-CSF). On d 5, the osteoclast number reached a maximum value. By d 15, the osteoclast number had decreased to about 70% of the maximum level. Moreover, by d 20, the osteoclast number had decreased to about 30% of its maximum level. On d 5, the osteoclast number of vitamin K2 12 h previously had decreased to about 30% of the M-CSF-only injected mice. Moreover, on d 5, the osteoclast number of the mice receiving a single injection of vitamin K2 24 h previously had decreased to about 15% that of mice injected only with M-CSF. These results indicate that vitamin K2 inhibits in vivo osteoclast formation. On d 20, the osteoclast number of the mice injected with a single dose of vitamin K2 12 or 24 h previously had decreased to 0% compared with those receiving only M-CSF. The present results suggest that the vitamin K2 "causes cell death" to mature osteoclasts and inhibits in vivo osteoclast formation.
机译：通过单次注射5微克重组人巨噬细胞集落刺激因子（M-CSF）即可治愈op / op小鼠中的破骨细胞缺乏症。在第5天，破骨细胞数达到最大值。到第15天，破骨细胞数量已降至最大水平的约70％。此外，到第20天，破骨细胞数量已降至其最大水平的约30％。在第5天，之前仅12小时注射M-CSF的小鼠的维生素K 2的破骨细胞数量已减少至约30％。而且，在第5天，先前24小时接受单次维生素K 2注射的小鼠的破骨细胞数量已降低至仅注射M-CSF的小鼠的破骨细胞数量的约15％。这些结果表明维生素K 2抑制体内破骨细胞形成。在第20天，与仅接受M-CSF的小鼠相比，之前单次注射维生素K2 12或24 h的小鼠的破骨细胞数量已降至0％。目前的结果表明，维生素K2“导致成熟的破骨细胞死亡”并抑制体内的破骨细胞形成。

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