Effect of magnolol on the function of osteoblastic MC3T3-E1 cells.

Abstract:

OBJECTIVES:In the present study, the ability of magnolol, a hydroxylated biphenyl compound isolated from Magnolia officinalis, to stimulate osteoblast function and inhibit the release of bone-resorbing mediators was investigated in osteoblastic MC3T3-E1 cells. METHODS:Osteoblast function was measured by cell growth, alkaline phosphatase activity, collagen synthesis, and mineralization. Glutathione content was also measured in the cells. Bone-resorbing cytokines, receptor activator of nuclear factor-κB ligand (RANKL), TNF-α, and IL-6 were measured with an enzyme immunoassay system. RESULTS:Magnolol caused a significant elevation of cell growth, alkaline phosphatase activity, collagen synthesis, mineralization, and glutathione content in the cells (P < 0.05). Skeletal turnover is orchestrated by a complex network of regulatory factors. Among cytokines, RANKL, TNF-α, and IL-6 were found to be key osteoclastogenetic molecules produced by osteoblasts. Magnolol significantly (P < 0.05) decreased the production of osteoclast differentiation inducing factors such as RANKL, TNF-α, and IL-6 in the presence of antimycin A, which inhibits mitochondrial electron transport and has been used as an ROS generator. CONCLUSION:Magnolol might be a candidate as an agent for the prevention of bone disorders such as osteoporosis.

journal_name

Mediators Inflamm

authors

Kwak EJ,Lee YS,Choi EM

doi

10.1155/2012/829650

subject

Has Abstract

pub_date

2012-01-01 00:00:00

pages

829650

eissn

0962-9351

issn

1466-1861

journal_volume

2012

pub_type

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