Triptolide Prevents Bone Destruction in the Collagen-Induced Arthritis Model of Rheumatoid Arthritis by Targeting RANKL/RANK/OPG Signal Pathway
Triptolide inhibits osteoclast differentiation by targeting RANKL/RANK/OPG signal pathway. Mice were orally administered triptolide (Trip, 8, 16, and 32 μg/kg, resp.), methotrexate (MTX, 0.1 mg/kg), or vehicle for 21 days from the first day of the onset of the clinical symptoms of arthritis. At the end of the experiment, the changes in RANKL, RANK, and OPG expression at both mRNA and protein levels in the ankle joint and serum were, respectively, detected by real-time PCR, immunohistochemistry, and ELISA assay. Triptolide reduces the expression of RANKL and RANK and enhances the expression of OPG and the ratio of RANKL to OPG in the ankle joint at mRNA (a) and protein (b) levels and in serum (c) of CIA mice. Data are represented as the mean ± SD (). in comparison with the normal control. , and in comparison with the vehicle control. , and in comparison with methotrexate-treated CIA mice.