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

Affiliation
Department of Orthopedic Surgery ,The Second Affiliated Hospital ,Zhejiang University School of Medicine ,Hangzhou City ,Zhejiang ,China
Yang, Guang;
Affiliation
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases ,National Clinical Research Center for Infectious Diseases ,Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases ,The First Affiliated Hospital ,College of Medicine ,Zhejiang University ,Hangzhou ,China
Xu, Huikang;
Affiliation
Department of Orthopedic Surgery ,The Second Affiliated Hospital ,Zhejiang University School of Medicine ,Hangzhou City ,Zhejiang ,China
Yao, Minjun;
Affiliation
Department of Orthopedic Surgery ,The Second Affiliated Hospital ,Zhejiang University School of Medicine ,Hangzhou City ,Zhejiang ,China
Yan, Shigui;
Affiliation
Department of Cell and Developmental Biology ,College of Life Sciences ,Zhejiang University ,Hangzhou ,China
Wu, Mengrui;
Affiliation
Department of Orthopedic Surgery ,The Second Affiliated Hospital ,Zhejiang University School of Medicine ,Hangzhou City ,Zhejiang ,China
Zhou, Chenhe

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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License Holder: Copyright © 2022 Yang, Xu, Yao, Yan, Wu and Zhou.

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