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

Kwak EJ, Lee YS, Choi EM - Mediators Inflamm. (2012)

Bottom Line: Magnolol caused a significant elevation of cell growth, alkaline phosphatase activity, collagen synthesis, mineralization, and glutathione content in the cells (P < 0.05).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.

View Article: PubMed Central - PubMed

Affiliation: Department of Food Science Technology, Yeungnam University, Gyeongsan 712-749, Republic of Korea.

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.

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Related in: MedlinePlus

Effect of magnolol on the alkaline phosphatase activity of MC3T3-E1 cells. Data were expressed as a percentage of control. The control value for ALP activity was 0.871 ± 0.016 Unit/mg. *P < 0.05 compared with control.
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fig3: Effect of magnolol on the alkaline phosphatase activity of MC3T3-E1 cells. Data were expressed as a percentage of control. The control value for ALP activity was 0.871 ± 0.016 Unit/mg. *P < 0.05 compared with control.

Mentions: MC3T3-E1 cells were incubated with magnolol and cell growth was measured. Cell populations cultured in basal or magnolol-treated media appeared as Figure 1. MC3T3-E1 cell growth was promoted by stimulation with magnolol (0.1~1 μM) significantly compared with control cells. The effect of magnolol on collagen synthesis in osteoblastic MC3T3-E1 cells is shown in Figure 2. The collagen synthesis of MC3T3-E1 cells was significantly increased by the addition of 0.1~1 μM magnolol. ALP activity was measured to study the effect of magnolol on the osteoblastic differentiation in MC3T3-E1 cells. The cultured cells in the presence of magnolol (0.1 and 1 μM) caused a significant increase in the ALP activity of osteoblastic cells (Figure 3). The MC3T3-E1 cells were treated with various concentrations of magnolol, and the mineralization of osteoblasts was measured. The increase of mineralization was significant at magnolol concentrations of 0.1 and 1 μM in MC3T3-E1 cell culture (Figure 4).


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

Kwak EJ, Lee YS, Choi EM - Mediators Inflamm. (2012)

Effect of magnolol on the alkaline phosphatase activity of MC3T3-E1 cells. Data were expressed as a percentage of control. The control value for ALP activity was 0.871 ± 0.016 Unit/mg. *P < 0.05 compared with control.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3306956&req=5

fig3: Effect of magnolol on the alkaline phosphatase activity of MC3T3-E1 cells. Data were expressed as a percentage of control. The control value for ALP activity was 0.871 ± 0.016 Unit/mg. *P < 0.05 compared with control.
Mentions: MC3T3-E1 cells were incubated with magnolol and cell growth was measured. Cell populations cultured in basal or magnolol-treated media appeared as Figure 1. MC3T3-E1 cell growth was promoted by stimulation with magnolol (0.1~1 μM) significantly compared with control cells. The effect of magnolol on collagen synthesis in osteoblastic MC3T3-E1 cells is shown in Figure 2. The collagen synthesis of MC3T3-E1 cells was significantly increased by the addition of 0.1~1 μM magnolol. ALP activity was measured to study the effect of magnolol on the osteoblastic differentiation in MC3T3-E1 cells. The cultured cells in the presence of magnolol (0.1 and 1 μM) caused a significant increase in the ALP activity of osteoblastic cells (Figure 3). The MC3T3-E1 cells were treated with various concentrations of magnolol, and the mineralization of osteoblasts was measured. The increase of mineralization was significant at magnolol concentrations of 0.1 and 1 μM in MC3T3-E1 cell culture (Figure 4).

Bottom Line: Magnolol caused a significant elevation of cell growth, alkaline phosphatase activity, collagen synthesis, mineralization, and glutathione content in the cells (P < 0.05).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.

View Article: PubMed Central - PubMed

Affiliation: Department of Food Science Technology, Yeungnam University, Gyeongsan 712-749, Republic of Korea.

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.

Show MeSH
Related in: MedlinePlus