Triptolide Prevents Bone Destruction in the Collagen-Induced Arthritis Model of Rheumatoid Arthritis by Targeting RANKL/RANK/OPG Signal Pathway release_znxar5ii3ncanns3a74iby7txm

by Chunfang Liu, Yanqiong Zhang, Xiangying Kong, Liuluan Zhu, Jian Pang, Ying Xu, Weiheng Chen, Hongsheng Zhan, Aiping Lu, Na Lin

Published in Evidence-Based Complementary and Alternative Medicine by Hindawi Limited.

2013   Volume 2013, p1-12

Abstract

Focal bone destruction within inflamed joints is the most specific hallmark of rheumatoid arthritis (RA). Our previous study indicated that the therapeutic efficiency of triptolide in RA may be due partially to its chondroprotective and anti-inflammatory effects. However, its roles in bone destruction are still unclear. In this study, our data firstly showed the therapeutic effects of triptolide on severity of arthritis and arthritis progression in collagen-induced arthritis (CIA) mice. Then, by micro-CT quantification, triptolide treatment significantly increased bone mineral density, bone volume fraction, and trabecular thickness and decreased trabecular separation of inflamed joints. Interestingly, triptolide treatment could prevent the bone destruction by reducing the number of osteoclasts in inflamed joints, reducing the expression of receptor activator of NF-<jats:italic>κ</jats:italic>B (RANK) ligand (RANKL) and RANK, increasing the expression of osteoprotegerin (OPG), at both mRNA and protein levels, and decreasing the ratio of RANKL to OPG in sera and inflamed joints of CIA mice, which were further confirmed in the coculture system of human fibroblast-like synovial and peripheral blood mononuclear cells. These findings offer the convincing evidence for the first time that triptolide may attenuate RA partially by preventing the bone destruction and inhibit osteoclast formation by regulating RANKL/RANK/OPG signal pathway.
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Type  article-journal
Stage   published
Year   2013
Language   en ?
DOI  10.1155/2013/626038
PubMed  23573139
PMC  PMC3610373
Wikidata  Q36723165
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