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首页> 外文期刊>International immunopharmacology >Tatarinan O, a lignin-like compound from the roots of Acorus tatarinowii Schott inhibits osteoclast differentiation through suppressing the expression of c-Fos and NFATc1
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Tatarinan O, a lignin-like compound from the roots of Acorus tatarinowii Schott inhibits osteoclast differentiation through suppressing the expression of c-Fos and NFATc1

机译:Tatarinan O,一种来自Acorus tatarinowii Schott根的木质素样化合物,可通过抑制c-Fos和NFATc1的表达来抑制破骨细胞分化

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摘要

Osteoclasts (OC) are large multinucleated cells derived from monocyte/macrophage precursors. Suppressing osteoclastogenesis is considered as an effective therapeutic approach to erosive bone disease. The root of Acorus tatarinowii Schott, a well-known traditional Chinese medicine was used to treat rheumatosis and other inflammatory disease. However, the effects of tatarinan O (TO), one of the lignin-like compounds isolated from the roots of Acorus tatarinowii Schott during bone development are still unclear. In the present study, we explored the effect of TO on RANKL-induced osteoclastogenesis in vitro. TO was found to suppress osteoclast differentiation from RANKL-stimulated mouse bone marrow macrophages (BMMs) without significant cytotoxicity. TO also dose dependently suppressed bone resorption activity of mature osteoclasts. Additionally, TO apparently inhibited the expression of osteoclastic marker genes, such as MMP-9, Cts K and TRAP. Furthermore, our results showed that TO decreased RANKL-induced expression of c-Fos and NFATc1 without influencing NF-kappa B activation and MAPK phosphorylation. Hence, for the first time we revealed that TO dose-dependently inhibited osteoclastogenesis from RANKL-stimulated mouse BMMs via decreasing the expression of NFATc1 and c-Fos. (C) 2016 Elsevier B.V. All rights reserved.
机译:破骨细胞(OC)是衍生自单核细胞/巨噬细胞前体的大型多核细胞。抑制破骨细胞形成被认为是治疗糜烂性骨疾病的有效方法。著名的中药Acorus tatarinowii Schott的根被用于治疗风湿病和其他炎性疾病。然而,塔塔林聚糖O(TO)的作用仍不清楚,塔塔林聚糖O(TO)是在骨骼发育过程中从Acorus tatarinowii Schott的根中分离出的一种木质素样化合物。在本研究中,我们探讨了TO对RANKL诱导的破骨细胞体外作用的影响。发现TO可抑制破骨细胞从RANKL刺激的小鼠骨髓巨噬细胞(BMM)分化,而没有明显的细胞毒性。 TO也剂量依赖性地抑制成熟破骨细胞的骨吸收活性。此外,TO明显抑制了破骨细胞标志物基因(如MMP-9,Cts K和TRAP)的表达。此外,我们的结果表明TO降低了RANKL诱导的c-Fos和NFATc1的表达,而不影响NF-κB的活化和MAPK磷酸化。因此,我们首次揭示了TO可以通过降低NFATc1和c-Fos的表达来剂量依赖性地抑制RANKL刺激的小鼠BMM的破骨细胞生成。 (C)2016 Elsevier B.V.保留所有权利。

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