Scholarlink

<p>Osteoporosis is a prevalent metabolic bone disease that requires multi-target therapeutic strategies. Formononetin (FMN), a bioactive isoflavone derived from Astragalus species, has shown potential in promoting bone health; however, its systemic mechanisms remain poorly understood. In this study, we evaluated the anti-osteoporotic effects of FMN using a glucocorticoid-induced bone loss model in zebrafish. Our results demonstrate that FMN significantly and dose-dependently promotes bone mineralization and effectively reverses glucocorticoid-induced skeletal damage. By integrating network pharmacology and molecular docking with experimental validation, we identified a multi-target mechanism underlying FMN's protective effects. FMN was found to regulate several key signaling pathways, including the PI3K-AKT and estrogen pathways, and its therapeutic impact was confirmed by the rectified expression of core genes involved in bone homeostasis and inflammation. This study reveals that FMN exerts its anti-osteoporotic effects through the coordinated regulation of growth factor signaling, calcium homeostasis, and the oxidative stress-bone metabolism axis. Our findings provide a systematic theoretical foundation for developing FMN as a promising natural therapeutic agent for osteoporosis through the modulation of osteoimmunology.</p> Graphical Abstract <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Formononetin attenuates glucocorticoid-induced osteoporosis via multiple osteoimmunological pathways: evidence from zebrafish and network pharmacology

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年8月3日

查看全文
  • Xuting Song,
  • Min He,
  • Jingran Cui,
  • Yiming Wang,
  • Zhenhai Cui,
  • Mengmeng Sun,
  • Meiying Jin

摘要

Osteoporosis is a prevalent metabolic bone disease that requires multi-target therapeutic strategies. Formononetin (FMN), a bioactive isoflavone derived from Astragalus species, has shown potential in promoting bone health; however, its systemic mechanisms remain poorly understood. In this study, we evaluated the anti-osteoporotic effects of FMN using a glucocorticoid-induced bone loss model in zebrafish. Our results demonstrate that FMN significantly and dose-dependently promotes bone mineralization and effectively reverses glucocorticoid-induced skeletal damage. By integrating network pharmacology and molecular docking with experimental validation, we identified a multi-target mechanism underlying FMN's protective effects. FMN was found to regulate several key signaling pathways, including the PI3K-AKT and estrogen pathways, and its therapeutic impact was confirmed by the rectified expression of core genes involved in bone homeostasis and inflammation. This study reveals that FMN exerts its anti-osteoporotic effects through the coordinated regulation of growth factor signaling, calcium homeostasis, and the oxidative stress-bone metabolism axis. Our findings provide a systematic theoretical foundation for developing FMN as a promising natural therapeutic agent for osteoporosis through the modulation of osteoimmunology.

Graphical Abstract