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Carnosol suppresses RANKL-induced osteoclastogenesis and attenuates titanium particles-induced osteolysis.
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2020-07-28 , DOI: 10.1002/jcp.29978
Yongxian Li 1, 2, 3, 4 , Sipeng Lin 5 , Panjie Liu 1, 2, 3 , Jianbin Huang 5 , Junxiong Qiu 5 , Zhenkang Wen 5 , Jinbo Yuan 4 , Heng Qiu 4 , Yuhao Liu 1, 2, 3, 4 , Qian Liu 6 , Tengpeng Zhou 1, 2, 3 , Peijie Luo 1, 2, 3 , Huizhi Guo 1, 2, 3 , Yanhuai Ma 1, 2, 3 , Danqing Guo 1, 2, 3 , Guoye Mo 2, 3 , Yongchao Tang 2, 3 , Liangliang Xu 1, 2, 3 , De Liang 2, 3 , Jiake Xu 4 , Yue Ding 5 , Shuncong Zhang 1, 2, 3
Affiliation  

Osteolysis is a common medical condition characterized by excessive activity of osteoclasts and bone resorption, leading to severe poor quality of life. It is essential to identify the medications that can effectively suppress the excessive differentiation and function of osteoclasts to prevent and reduce the osteolytic conditions. It has been reported that Carnosol (Car), isolated from rosemary and salvia, has anti‐inflammatory, antioxidative, and anticancer effects, but its activity on osteolysis has not been determined. In this study, we found that Car has a strong inhibitory effect on the receptor activator of nuclear factor‐κB ligand (RANKL)‐induced osteoclast differentiation dose‐dependently without any observable cytotoxicity. Moreover, Car can inhibit the RANKL‐induced osteoclastogenesis and resorptive function via suppressing NFATc1, which is a result of affecting MAPK, NF‐κB and Ca2+ signaling pathways. Moreover, the particle‐induced osteolysis mouse model confirmed that Car could be effective for the treatment of bone loss in vivo. Taken together, by suppressing the formation and function of RANKL‐induced osteoclast, Car, may be a therapeutic supplementary in the prevention or the treatment of osteolysis.

中文翻译:


鼠尾草酚抑制 RANKL 诱导的破骨细胞生成并减弱钛颗粒诱导的骨溶解。



骨质溶解是一种常见的疾病,其特征是破骨细胞过度活跃和骨吸收,导致严重的生活质量差。有必要找到能够有效抑制破骨细胞过度分化和功能的药物,以预防和减少溶骨性疾病。据报道,从迷迭香和丹参中分离出来的鼠尾草酚(Car)具有抗炎、抗氧化和抗癌作用,但其对骨质溶解的活性尚未确定。在这项研究中,我们发现 Car 对核因子 κB 配体受体激活剂 (RANKL) 诱导的破骨细胞分化具有剂量依赖性的强烈抑制作用,且没有任何可观察到的细胞毒性。此外,Car 可以通过抑制 NFATc1 来抑制 RANKL 诱导的破骨细胞生成和骨吸收功能,这是影响 MAPK、NF-κB 和 Ca 2+信号通路的结果。此外,颗粒诱导的骨质溶解小鼠模型证实,Car 可有效治疗体内骨质流失。综上所述,通过抑制 RANKL 诱导的破骨细胞的形成和功能,Car 可能成为预防或治疗骨溶解的治疗补充剂。
更新日期:2020-07-28
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