Kawata T, Zernik J H, Fujita T, Tokimasa C, Tanne K
Department of Orthodontics, Hiroshima University School of Dentistry, Japan.
J Nutr Sci Vitaminol (Tokyo). 1999 Aug;45(4):501-7. doi: 10.3177/jnsv.45.501.
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.
单次注射5微克重组人巨噬细胞集落刺激因子（M-CSF）可治愈op/op小鼠的破骨细胞缺乏症。在第5天，破骨细胞数量达到最大值。到第15天，破骨细胞数量已降至最大值的约70%。此外，到第20天，破骨细胞数量已降至最大值的约30%。在第5天，提前12小时注射维生素K2的小鼠破骨细胞数量已降至仅注射M-CSF小鼠的约30%。此外，在第5天，提前24小时单次注射维生素K2的小鼠破骨细胞数量已降至仅注射M-CSF小鼠的约15%。这些结果表明维生素K2在体内抑制破骨细胞形成。在第20天，提前12或24小时注射单剂量维生素K2的小鼠破骨细胞数量与仅接受M-CSF的小鼠相比已降至0%。目前的结果表明维生素K2使成熟破骨细胞“发生细胞死亡”并在体内抑制破骨细胞形成。
