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

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 s...

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Published inFrontiers in pharmacology Vol. 13; p. 1019478
Main Authors Yang, Guang, Xu, Huikang, Yao, Minjun, Yan, Shigui, Wu, Mengrui, Zhou, Chenhe
Format Journal Article
LanguageEnglish
Published Frontiers Media S.A 03.11.2022
Subjects
ERK
NLRP3 inflammasome
norcantharidin
osteoclast
osteoporosis
Pharmacology
ROS
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Summary: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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Reviewed by: Xin Wei, University of Nebraska Medical Center, United States
Zhiguo Zhang, Institute of Basic Theory, China Academy of Chinese Medical Sciences, China
Edited by: Gary Xiao, Dalian University of Technology, China
This article was submitted to Experimental Pharmacology and Drug Discovery, a section of the journal Frontiers in Pharmacology
ISSN:1663-9812
1663-9812
DOI:10.3389/fphar.2022.1019478