Protective effect of VK(2) on glucocorticoid-treated MC3T3-E1 cells

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 K(2) (VK(2)) has been proven to promote bone formation both in vitro and in vivo. In this study, we examined the effects of VK(2) on dexamethasone (DEX)-treated MC3T3-E1 osteoblastic cells. We observed that VK(2) promoted the proliferation and enhanced the survival of dexamethasone-treated MC3T3-E1 cells. In addition, VK(2) 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 VK(2) 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.