Effect of Magnolol on the Function of Osteoblastic MC3T3-E1 Cells

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 measu...

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Main Authors: Eun Jung Kwak, Young Soon Lee, Eun Mi Choi
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2012/829650
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author Eun Jung Kwak
Young Soon Lee
Eun Mi Choi
author_facet Eun Jung Kwak
Young Soon Lee
Eun Mi Choi
author_sort Eun Jung Kwak
collection DOAJ
description 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.
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spelling doaj-art-f128e3a09279424ea175ffae217c06912025-02-03T05:59:52ZengWileyMediators of Inflammation0962-93511466-18612012-01-01201210.1155/2012/829650829650Effect of Magnolol on the Function of Osteoblastic MC3T3-E1 CellsEun Jung Kwak0Young Soon Lee1Eun Mi Choi2Department of Food Science Technology, Yeungnam University, Gyeongsan 712-749, Republic of KoreaDepartment of Food & Nutrition, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of KoreaDepartment of Food & Nutrition, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of KoreaObjectives. 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.http://dx.doi.org/10.1155/2012/829650
spellingShingle Eun Jung Kwak
Young Soon Lee
Eun Mi Choi
Effect of Magnolol on the Function of Osteoblastic MC3T3-E1 Cells
Mediators of Inflammation
title Effect of Magnolol on the Function of Osteoblastic MC3T3-E1 Cells
title_full Effect of Magnolol on the Function of Osteoblastic MC3T3-E1 Cells
title_fullStr Effect of Magnolol on the Function of Osteoblastic MC3T3-E1 Cells
title_full_unstemmed Effect of Magnolol on the Function of Osteoblastic MC3T3-E1 Cells
title_short Effect of Magnolol on the Function of Osteoblastic MC3T3-E1 Cells
title_sort effect of magnolol on the function of osteoblastic mc3t3 e1 cells
url http://dx.doi.org/10.1155/2012/829650
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