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<p>Long-term treatment with glucocorticoids significantly impacts bone health, with glucocorticoid-induced osteoporosis (GIOP) being the most prevalent consequence. Previous studies have established that Atractylenolide I (Atr I) possesses anti-inflammatory, antioxidant and anti-tumor properties, however, its specific effects on osteoclastogenesis and GIOP are still unclear. In this study, our in vitro results revealed that Atr I inhibited RANKL-stimulated osteoclast differentiation in a dose-dependent manner, disrupted the structure of the F-actin belt in mature osteoclasts, blocked RANKL-induced ROS production, and suppressed the expression of osteoclast-associated genes. Mechanistically, the findings indicated that Atr I inhibited the RANKL-induced activation of the NF-κB signaling pathway. In vivo, the micro-CT, bone histomorphometric analysis and histological data demonstrated that Dex administration led to significant bone loss, accompanied by a considerable increase in the number of osteoclasts on the bone surface. Conversely, treatment with Atr I effectively prevented these Dex-induced alterations. Taken together, this study suggests that Atr I may hold potential as a therapeutic agent for the treatment of GIOP.</p>

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Atractylenolide I Attenuates Glucocorticoid-Induced Osteoporosis via Inhibiting NF-κB Signaling Pathway

  • 期刊论文

  • 发表日期：

    2025年3月12日

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  • Yamei Liu,
  • Xiaoqi Deng,
  • Chen Chen,
  • Binlan Fu,
  • Min Wang,
  • Jinglan Li,
  • Liangliang Xu,
  • Bin Wang

摘要

Long-term treatment with glucocorticoids significantly impacts bone health, with glucocorticoid-induced osteoporosis (GIOP) being the most prevalent consequence. Previous studies have established that Atractylenolide I (Atr I) possesses anti-inflammatory, antioxidant and anti-tumor properties, however, its specific effects on osteoclastogenesis and GIOP are still unclear. In this study, our in vitro results revealed that Atr I inhibited RANKL-stimulated osteoclast differentiation in a dose-dependent manner, disrupted the structure of the F-actin belt in mature osteoclasts, blocked RANKL-induced ROS production, and suppressed the expression of osteoclast-associated genes. Mechanistically, the findings indicated that Atr I inhibited the RANKL-induced activation of the NF-κB signaling pathway. In vivo, the micro-CT, bone histomorphometric analysis and histological data demonstrated that Dex administration led to significant bone loss, accompanied by a considerable increase in the number of osteoclasts on the bone surface. Conversely, treatment with Atr I effectively prevented these Dex-induced alterations. Taken together, this study suggests that Atr I may hold potential as a therapeutic agent for the treatment of GIOP.