Protective effect of VK2 on glucocorticoid-treated MC3T3-E1 cells.

Protective effect of VK2 on glucocorticoid-treated MC3T3-E1 cells.
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VK2对糖皮质激素处理的MC3T3-E1细胞的保护作用

DOI:
10.3892/ijmm.2016.2817
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发表时间:
2017-01
影响因子:
5.4
通讯作者:
Gao YS
Gao YS
中科院分区:
医学3区
文献类型:
--
作者:
Zhang YL;Yin JH;Ding H;Zhang W;Zhang CQ;Gao YS

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糖皮质激素 (GC) 会导致继发性骨质疏松症和骨坏死的发生率增加,用于预防和治疗这些并发症的药物已被研究多年。维生素 K2 (VK2) 已被证明可以在体外和体内促进骨形成。在这项研究中,我们检查了 VK2 对地塞米松 (DEX) 处理的 MC3T3-E1 成骨细胞的影响。我们观察到 VK2 促进地塞米松处理的 MC3T3-E1 细胞的增殖并增强其存活率。此外,VK2上调成骨标志蛋白的表达水平,如Runt相关转录因子2(Runx2)、碱性磷酸酶(ALP)和骨钙素,而这些蛋白被地塞米松显着抑制。总的来说,我们的研究结果表明,VK2有潜力拮抗GC对MC3T3-E1细胞的影响,因此可能被证明是预防和治疗GC诱导的骨质疏松症和骨坏死的有前途的药物。
Glucocorticoids (GCs) contribute to the increased incidence of secondary osteoporosis and osteonecrosis, and medications for the prevention and treatment of these complications have been investigated for many years. Vitamin K2 (VK2) has been proven to promote bone formation both in vitro and in vivo. In this study, we examined the effects of VK2 on dexamethasone (DEX)-treated MC3T3-E1 osteoblastic cells. We observed that VK2 promoted the proliferation and enhanced the survival of dexamethasone-treated MC3T3-E1 cells. In addition, VK2 upregulated the expression levels of osteogenic marker proteins, such as Runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP) and osteocalcin, which were significantly inhibited by dexamethasone. On the whole, our findings indicate that VK2 has the potential to antagonize the effects of GCs on MC3T3-E1 cells, and may thus prove to be a promising agent for the prevention and treatment of GC-induced osteoporosis and osteonecrosis.
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