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Merck

Stimulatory effects of platycodin D on osteoblast differentiation.

Journal of cellular biochemistry (2019-03-20)
Younho Han, Sun Woo Jin, Gi Ho Lee, Jae Ho Choi, Hyun Sun Lee, Young Chul Chung, Hye Gwang Jeong, Kwang Youl Lee
ABSTRACT

Previous studies have suggested that platycodin D is implicated in bone biology and ameliorates osteoporosis development. Platycodin D repressed the osteoclast activity and enhanced bone mineral density in the mouse model. However, the effects of platycodin D on osteoblast differentiation have not been elucidated yet. In C3H10T1/2 cells, platycodin D upregulated osteogenic markers including alkaline phosphatase (ALP), bone sialoprotein, and collagen type 1 alpha 1, and transcription factors, such as Runx2 and osterix, subsequently enhancing the bone mineralization. In a molecular mechanism study, platycodin D induced β-catenin nuclear accumulation by upregulating GSK3β phosphorylation. Furthermore, platycodin D upregulated the ALP activity and enhanced the mineralization process in osteoblast cells via the sirtuin 1/β-catenin pathways. Taken together, these results suggested that platycodin D could be an effective therapeutic compound against osteoporosis because of its regulatory effects during the osteoblast differentiation.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Sirtinol, A cell-permeable 2-hydroxy-1-naphthaldehyde derivative that acts as a specific and direct inhibitor of the sirtuin class of deacetylase activity with no affect on human HDAC1.
Sigma-Aldrich
Anti-β-Catenin antibody produced in rabbit, whole antiserum