php0034 rankl,原硅酸对RANKL刺激RAW264.7细胞破骨形成的抑制作用

【摘要】

Numerous studies have reported on the positive effects of silicon (Si) on bone metabolism, particularly on the stimulatory effects of Si on osteoblast cells and on bone formation. Inhibitory effects of Si on osteoclast formation and bone resorption have also been demonstrated in vitro and are suggested to be mediated indirectly via stromal and osteoblast cells. Direct effects of Si on osteoclasts have been less studied and mostly using soluble Si, but no characterisation of the Si treatment solutions are provided. The aims of the present study were to (a) further investigate the direct inhibitory effects of Si on osteoclastogenesis in RANKL‐stimulated RAW264.7 cells, (b) determine at what stage during osteoclastogenesis Si acts upon, and (c) determine if these effects can be attributed to the biologically relevant soluble orthosilicic acid specie. Our results demonstrate that silicon, at 50 μg/ml (or 1.8 mM), does not affect cell viability but directly inhibits the formation of TRAP+ multinucleated cells and the expression of osteoclast phenotypic genes in RAW264.7 cells. The inhibitory effect of Si was clearly associated with the early stages (first 24 hr) of osteoclastogenesis. Moreover, these effects can be attributed to the soluble orthosilicic acid specie.

大量研究报道了硅(Si)对骨代谢的积极作用，特别是硅对成骨细胞和骨形成的促进作用。体外实验也证实了硅对破骨细胞形成和骨吸收的抑制作用，并认为硅是通过基质细胞和成骨细胞间接介导的。硅对破骨细胞的直接影响研究较少，主要使用可溶性硅，但没有提供硅处理溶液的表征。本研究的目的是(a)进一步研究Si的直接抑制作用在RANKL osteoclastogenesis RAW264.7细胞进行刺激量,(b)确定在哪个阶段osteoclastogenesis Si行为,和(c)确定这些影响可以归因于生物相关的可溶性原硅酸的形式。我们的结果表明，50 μg/ml(或1.8 mM)的硅不会影响细胞活力，而是直接抑制RAW264.7细胞中TRAP+多核细胞的形成和破骨细胞表型基因的表达。Si的抑制作用与破骨形成的早期(前24小时)明显相关。此外，这些影响可归因于可溶性原硅酸物种。[翻译仅供参考]