...
首页> 外文期刊>Journal of Cellular Physiology >Luteoloside prevents lipopolysaccharide‐induced osteolysis and suppresses RANKL‐induced osteoclastogenesis through attenuating RANKL signaling cascades
【24h】

Luteoloside prevents lipopolysaccharide‐induced osteolysis and suppresses RANKL‐induced osteoclastogenesis through attenuating RANKL signaling cascades

机译:Luteoloside阻止脂多糖诱导骨质溶解,抑制RANKL诱导通过衰减osteoclastogenesis RANKL信号级联

获取原文
获取原文并翻译 | 示例
           

摘要

Bone destruction or osteolysis marked by excessive osteoclastic bone resorption is a very common medical condition. Identification of agents that can effectively suppress excessive osteoclast formation and function is crucial for prevention and treatment of osteolytic conditions such as periprosthetic joint infection and periprosthetic loosening. Luteoloside, a flavonoid, is a natural bioactive compound with anti‐inflammation and anti‐tumor properties. However, the effect of Luteoloside on inflammation‐induced osteolysis is unknown. Here, we found that Luteoloside exhibited a strong inhibitory effect on lipopolysaccharide (LPS)‐induced osteolysis in vivo. In addition, Luteoloside suppressed RANKL‐induced osteoclast differentiation and abrogated bone resorption in a dose‐dependent manner. Further, we found that the anti‐osteoclastic and anti‐resorptive actions of Luteoloside are mediated via blocking NFATc1 activity and the attenuation of RANKL‐mediated Ca 2+ signaling as well as NF‐κB and MAPK pathways. Taken together, this study shows that Luteoloside may be a potential therapeutic agent for osteolytic bone diseases associated with abnormal osteoclast formation and function in inflammatory conditions.
机译:骨破坏或骨质溶解过度监测骨吸收是非常常见的医疗条件。能有效抑制破骨细胞过度形成和功能是预防的关键和治疗溶骨的条件等periprosthetic联合感染和periprosthetic放松。生物活性化合物与抗炎症和抗肿瘤特性。Luteoloside所致炎症诱导骨质溶解未知的。表现出强烈的抑制作用脂多糖(LPS)诱导的骨质溶解vivoRANKL的诱导破骨细胞分化和废除骨吸收的剂量依赖性的方式。反的监测和抗再吸收的行动通过阻断NFATc1 Luteoloside是介导活动和RANKL介导应承担的Ca的衰减2 +信号以及NFκB和MAPK通路。综上所述,本研究表明Luteoloside可能是一个潜在的治疗代理吗溶骨的骨疾病与异常有关破骨细胞形成和功能在炎症条件。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号