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Effects of Silicon on Inhibition of Oxidative Stress and Inflammatory Mediator during Bone Metabolism
Author(s) -
Choi Mi-Kyeong,
Kim Eun-Jin,
Bu So-Young,
Sung Mi-Kyung
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb277
Subject(s) - chemistry , osteoclast , oxidative stress , bone remodeling , viability assay , inflammation , apoptosis , medicine , in vitro , biochemistry
The purpose of this study was to investigate the effect of silicon (Si) on the production of DPPH free radicals and inflammatory mediators, and identify the role of Si in bone formation and osteoclastogenesis in vitro. The murine macrophage cell line (RAW 264.7) was utilized as osteoclast precursor cells and the production of inflammatory mediators was measured. Cells were plated for 6 hours, stimulated with either LPS (10 ng/ml) as an inflammatory reagent or LPS with Si (1, 5, 10, 25, 50 uM), doses of which does not affect cell viability. By 24 and 48 hrs treatment, Si dose‐dependently decreased the LPS‐induced NO production by as much as 50%. All doses of Si decreased DPPH radical scavenging activities. In MC3T3‐E1 murine ostetoblast like cells, 1, 2.5 and 5 uM of Si significantly increased intracellular ALP activity under normal conditions at 7 days of Si treatment (p<0.05). Also two high doses of Si (25 and 50 uM) increased mineralized nodules formation at 14 days of differentiation as evidenced by increased Alizarin red S staining. We conclude that Si have positive effect on bone metabolism by increasing bone formation and possibly regulating osteoclastogenesis through its anti‐oxidative and anti‐inflammatory properties. “This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2011‐0010880)”