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首页> 外文期刊>Journal of Cellular Physiology >Eriodictyol Inhibits RANKL-Induced Osteoclast Formation and Function Via Inhibition of NFATc1 Activity
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Eriodictyol Inhibits RANKL-Induced Osteoclast Formation and Function Via Inhibition of NFATc1 Activity

机译：圣草酚抑制RANKL-Induced破骨细胞通过抑制NFATc1形成和功能活动

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摘要

Receptor activator of nuclear factor kappa-B ligand (RANKL) induces differentiation and function of osteoclasts through triggering multiple signaling cascades, including NF-kappa B, MAPK, and Ca2+-dependent signals, which induce and activate critical transcription factor NFATc1. Targeting these signaling cascades may serve as an effective therapy against osteoclast-related diseases. Here, by screening a panel of natural plant extracts with known anti-inflammatory, anti-tumor, or anti-oxidant properties for possible anti-osteoclastogenic activities we identified Eriodictyol. This flavanone potently suppressed RANKL-induced osteoclastogenesis and bone resorption in a dose-dependent manner without detectable cytotoxicity, suppressing RANKL-induced NF-kappa B, MAPK, and Ca2+ signaling pathways. Eriodictyol also strongly inhibited RANKL-induction of c-Fos levels (a critical component of AP-1 transcription factor required by osteoclasts) and subsequent activation of NFATc1, concomitant with reduced expression of osteoclast specific genes including cathepsin K (Ctsk), V-ATPase-d2 subunit, and tartrate resistant acid phosphatase (TRAcP/Acp5). Taken together, these data provide evidence that Eriodictyol could be useful for the prevention and treatment of osteolytic disorders associated with abnormally increased osteoclast formation and function. (C) 2016 Wiley Periodicals, Inc.
机译：kappa-B受体激活核因素配体(RANKL)诱导分化破骨细胞通过触发的函数多个信号级联,包括nf -κB、MAPK和Ca2 +端依赖信号,诱导并激活关键转录因子NFATc1。作为一个有效的疗法osteoclast-related疾病。面板的天然植物提取物抗炎,抗肿瘤,抗氧化属性可能anti-osteoclastogenic我们确定了圣草酚的活动。黄烷酮强有力地抑制RANKL-inducedosteoclastogenesis和骨吸收剂量依赖性的方式没有检测到细胞毒性,抑制RANKL-induced nf -κB、MAPK和Ca2 +信号通路。还强烈抑制RANKL-induction c-Fos水平(AP-1的一个重要组成部分破骨细胞)和所需的转录因子随后激活NFATc1,相伴减少破骨细胞特定基因的表达包括组织蛋白酶K (Ctsk), V-ATPase-d2亚基、抗酒石酸酸性磷酸酶(TRAcP / Acp5)。证据表明,圣草酚可能是有用的预防和治疗溶骨的障碍与异常增加破骨细胞相关形成和功能。期刊、公司。

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