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首页> 外文期刊>The Journal of Nutritional Biochemistry >Fisetin antagonizes cell fusion, cytoskeletal organization and bone resorption in RANKL-differentiated murine macrophages
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Fisetin antagonizes cell fusion, cytoskeletal organization and bone resorption in RANKL-differentiated murine macrophages

机译：Fisetin拮抗RANKL分化的鼠巨噬细胞中的细胞融合，细胞骨架组织和骨吸收。

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Osteoclastogenesis is comprised of several stage s including progenitor survival, differentiation to mononuclear preosteoclasts, cell fusion to multinuclear mature osteoclasts, and activation to osteoclasts with bone resorbing activity. Botanical antioxidants are now being increasingly investigated for their health-promoting effects on bone. This study investigated that fisetin, a flavonol found naturally in many fruits and vegetables, suppressed osteoclastogenesis by disturbing receptor activator of nuclear factor (NF)-kappa B ligand (RANKL)-mediated signaling pathway and demoting osteoclastogenic protein induction. Nontoxic fisetin at = 10 mu M inhibited the induction of RANK, tumor necrosis factor receptor associated factor 6 (TRAF6) and the activation of NF-kappa B in RANKL-stimulated RAW 264.7 macrophages. In RANKL-differentiated osteoclasts cell fusion protein of E-cadherin was induced, which was dampened by fisetin. The formation of tartrate-resistance acid phosphatase-positive multinucleated osteoclasts was suppressed by adding fisetin to RANKL-exposed macrophages. It was also found that fisetin reduced actin ring formation and gelsolin induction of osteclasts enhanced by RANKL through disturbing c-Src-proline-rich tyrosine kinase 2 signaling. Fisetin deterred preosteoclasts from the cell-cell fusion and the organization of the cytoskeleton to seal the resorbing area and to secret protons for bone resorption. Consistently, the 5 day-treatment of fisetin diminished RANKL-induced cellular expression of carbonic anhydrase II and integrin 33 concurrently with a reduction of osteoclast bone-resorbing activity. Therefore, fisetin was a natural therapeutic agent retarding osteoclast fusion and cytoskeletal organization such as actin rings and ruffled boarder, which is a property of mature osteoclasts and is required for osteoclasts to resorb bone. (C) 2014 Elsevier Inc. All rights reserved.
机译：破骨细胞形成包括几个阶段，包括祖细胞存活，分化为单核破骨细胞，细胞融合为多核成熟破骨细胞以及激活具有骨吸收活性的破骨细胞。植物抗氧化剂对骨骼的健康促进作用目前正在受到越来越多的研究。这项研究调查了菲塞汀（一种在许多水果和蔬菜中天然发现的黄酮醇）通过干扰核因子（NF）-κB配体（RANKL）介导的信号通路的受体激活剂并降低破骨细胞生成蛋白的诱导而抑制了破骨细胞的生成。 <= 10μM的无毒非瑟酮在RANKL刺激的RAW 264.7巨噬细胞中抑制RANK，肿瘤坏死因子受体相关因子6（TRAF6）的诱导和NF-κB的激活。在RANKL分化的破骨细胞中，诱导了E-钙粘着蛋白的细胞融合蛋白，该蛋白被非瑟酮抑制。通过向暴露于RANKL的巨噬细胞中添加非瑟酮抑制了酒石酸抵抗酸性磷酸酶阳性多核破骨细胞的形成。还发现，fisetin通过干扰富含c-Src-脯氨酸的酪氨酸激酶2信号传导，减少了RANKL增强的肌动蛋白环形成和凝溶胶蛋白诱导的破骨细胞。 Fisetin阻止了细胞与细胞融合以及细胞骨架的组织形成的破骨细胞，从而封闭了吸收区域并分泌了质子用于骨吸收。一致地，非瑟定的5天治疗减少了RANKL诱导的碳酸酐酶II和整联蛋白33的细胞表达，同时降低了破骨细胞的骨吸收活性。因此，非瑟定是延迟破骨细胞融合和细胞骨架组织的天然治疗剂，例如肌动蛋白环和褶皱的寄宿生，这是成熟的破骨细胞的特性，是破骨细胞吸收骨骼的必需物质。 （C）2014 Elsevier Inc.保留所有权利。

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