Norcantharidin ameliorates estrogen deficient-mediated bone loss by attenuating the activation of extracellular signal-regulated kinase/ROS/NLRP3 inflammasome signaling.

Norcantharidin ameliorates estrogen deficient-mediated bone loss by attenuating the activation of extracellular signal-regulated kinase/ROS/NLRP3 inflammasome signaling.
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DOI:
10.3389/fphar.2022.1019478
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发表时间:
2022
影响因子:
5.6
通讯作者:
--
中科院分区:
医学2区
文献类型:
--
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骨质疏松症的特征是骨量减少、骨结构异常和骨脆性升高,其由骨吸收和骨形成之间的骨稳态破坏所驱动。然而,到目前为止,没有一种药物是完美的骨质疏松症治疗,由于不同的缺陷。在这项研究中,我们证明了去甲斑蝥素(NCTD)可以抑制破骨细胞的形成和骨吸收,通过减弱ERK,ROS和NLRP3炎症体途径在体外。此外,我们的体内研究进一步证实了其通过抑制破骨细胞的形成和功能对雌激素缺乏性骨丢失的预防作用。因此,我们可以得出结论,NCTD可能是预防和治疗骨质疏松症的潜在候选者。
Osteoporosis, characterized by reduced bone mass, aberrant bone architecture, and elevated bone fragility, is driven by a disruption of bone homeostasis between bone resorption and bone formation. However, up to now, no drugs are perfect for osteoporosis treatment due to different defects. In this study, we demonstrated that norcantharidin (NCTD) could inhibit osteoclast formation and bone resorption by attenuating the ERK, ROS and NLRP3 inflammasomes pathways in vitro. Moreover, our in vivo study further confirms its preventive effects on estrogen-deficiency bone loss by inhibiting osteoclast formation and functions. Therefore, we could conclude that NCTD might be a potential candidates for the prevention and treatment of osteoporosis.
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