炎症性疾病常常因持续炎症而导致骨质流失，炎症会激活破骨细胞并增加骨吸收。氧化槐果碱 (OSC) 是一种从槐花和其他豆科植物根中提取的生物碱，具有神经保护和抗肿瘤特性。然而，OSC是否能有效抑制破骨细胞的分化和骨吸收尚不确定。因此，本研究探讨了OSC在破骨细胞形成和炎症性骨溶解中的潜在作用及其潜在机制。本研究涉及使用巨噬细胞集落刺激因子（M-CSF）和受体激活剂诱导原代小鼠骨髓巨噬细胞（BMM）进入破骨细胞。 NF-κB 配体 (RANKL) 并检查了 OSC 对破骨细胞 (OC) 分化、功能和细胞内活性氧 (ROS) 产生的影响。使用实时定量 PCR 评估 OSC 对破骨细胞特异性基因和炎症相关因子表达的影响。此外，还使用蛋白质印迹法检查了氧化应激相关因子、NF-κB 和 MAPK 信号通路的变化。最后，本研究探讨了OSC对体内钛（Ti）颗粒诱导的小鼠颅骨吸收模型的影响。OSC抑制OC分化和吸收，降低细胞内ROS水平。此外，OSC 抑制 IL-1β、TNF-α、IL-6 和破骨细胞特异性基因转录，同时增加 Nrf2 和 HO-1 蛋白表达。此外，OSC 抑制 NFATc1 基因的表达和自动调节，最终导致 Ti 颗粒诱导的小鼠骨吸收减少。OSC 可以被视为治疗破骨细胞相关炎症性溶骨性疾病的创新药物。© 2024。作者获得 Springer Nature Switzerland AG 的独家许可。

Inflammatory diseases often result in bone loss due to persistent inflammation, which activates osteoclasts and increases bone resorption. Oxysophocarpine (OSC), a bioalkaloid extracted from the roots of Sophora japonica and other leguminous plants, has neuroprotective and anti-tumor properties. However, it is still uncertain whether OSC can effectively inhibit the differentiation of osteoclasts and bone resorption. Therefore, this study explored the potential role of OSC in osteoclast formation and inflammatory osteolysis and its underlying mechanisms.This study involved inducing primary mouse bone marrow macrophages (BMMs) into osteoclasts using macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL) and examined the effects of OSC on osteoclast (OC) differentiation, function, and intracellular reactive oxygen species (ROS) production. The impact of OSC on the expression of osteoclast-specific genes and inflammation-related factors was assessed using real-time quantitative PCR. Additionally, changes in oxidative stress-related factors, NF-κB, and MAPK signaling pathways were examined using western blotting. Finally, this study investigated the influence of OSC on a mouse cranial bone resorption model induced by titanium (Ti) particles in vivo.OSC inhibited OC differentiation and resorption and reduces intracellular ROS levels. Moreover, OSC suppressed IL-1β, TNF-α, IL-6, and osteoclast-specific gene transcription while increasing Nrf2 and HO-1 protein expression. Furthermore, OSC inhibited the expression and autoregulation of the NFATc1 gene, ultimately leading to a reduction in Ti particle-induced bone resorption in mice.OSC could be regarded as an innovative medication for the treatment of osteoclast-associated inflammatory osteolytic diseases.© 2024. The Author(s), under exclusive licence to Springer Nature Switzerland AG.