Maackiain通过减弱rankl刺激的NF-κB信号通路和NFATc1活性来抑制破骨细胞的发生。

IF 5.3 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Journal of Cellular and Molecular Medicine Pub Date : 2020-11-01 Epub Date: 2020-09-16 DOI:10.1111/jcmm.15647
Yuhao Liu, Weizai Zeng, Chao Ma, Ziyi Wang, Chao Wang, Shaobin Li, Wei He, Qingwen Zhang, Jiake Xu, Chi Zhou
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引用次数: 12

摘要

溶骨病以破骨细胞形成和吸收功能过度增强为特征,对人体健康有重大影响。抑制破骨细胞分化和功能是临床治疗溶骨疾病的关键策略。麻黄素是一种从苦参中提取的天然化合物,已被用于抗过敏和抗肿瘤治疗。本研究结果表明,Maackiain对核因子-κB配体受体激活因子(RANKL)刺激的破骨细胞形成和羟基磷灰石吸收具有剂量依赖性,并能中断成熟破骨细胞F-actin带的结构。它还抑制破骨细胞特异性基因和蛋白质的表达。此外,Maackiain可以抑制rankl刺激的NF-κB和钙信号通路,抑制活化T细胞胞质核因子1活性、蛋白表达和向核转运。这些结果表明,Maackiain可能对破骨细胞相关疾病有潜在的治疗作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Maackiain dampens osteoclastogenesis via attenuating RANKL-stimulated NF-κB signalling pathway and NFATc1 activity.

Osteolytic diseases are typified by over-enhanced formation and resorbing function of osteoclasts and have a major impact on human health. Inhibition of osteoclastic differentiation and function is a key strategy for clinical therapy of osteolytic conditions. Maackiain is a natural compound extracted from Sophora flavescens, which has been applied to anti-allergic and anti-tumour treatments. The present results showed that Maackiain could restrain receptor activator of nuclear factor-κB ligand (RANKL)-stimulated osteoclast formation and hydroxyapatite resorption dose-dependently, and interrupt the structures of F-actin belts in the mature osteoclasts. It also repressed the expressions of osteoclast-specific genes and proteins. Furthermore, Maackiain could inhibit RANKL-stimulated NF-κB and calcium signalling pathways, and dampen Nuclear factor of activated T cell cytoplasmic 1 activity, protein expression and translocation into the nucleus. These results revealed that Maackiain may have a potential therapeutic effect on osteoclast-related disorders.

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来源期刊
CiteScore
10.00
自引率
1.90%
发文量
496
审稿时长
28 weeks
期刊介绍: Bridging physiology and cellular medicine, and molecular biology and molecular therapeutics, Journal of Cellular and Molecular Medicine publishes basic research that furthers our understanding of the cellular and molecular mechanisms of disease and translational studies that convert this knowledge into therapeutic approaches.
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