Alleviation of osteoarthritis by calycosin-7-O-β-D-glucopyranoside (CG) isolated from Astragali radix (AR) in rabbit osteoarthritis (OA) model

Objective: This work was undertaken to assess the protective effect of an isoflavonoid, calycosin-7-O-beta-D-glucopyranoside (CG), isolated from Astragali radix (AR) on the pathogenesis of osteoarthritis (OA)-like lesion in a rabbit model. Methods: Nine rabbits underwent an anterior cruciate ligament and menisectomy transection (ACLMT) of the rear knee joints to induce OA-like lesion. They were randomly divided into three groups (n = 6/group): a negative control group treated with 200 mu l of 0.5% (v/v) dimethyl sulfoxide (DMSO), a positive control group treated with 200 VI of 100 mu M piroxicam, and a test group treated with 100 mu g/500 mu l of CG, where the test agents were administered by injection once a week for 4 weeks starting from the third week. Rabbits were then sacrificed to observe the progression of OA-like lesion. The synovial fluid was analyzed for the amounts of total proteins, glycosaminoglycans (GAG) and prostaglandin E-2 (PGE(2)). In addition, histopathologic analyses were performed on the OA-like articular cartilage with or without therapeutic treatments. Results: The total synovial fluid volume (P < 0.05) was most strikingly reduced by the treatment with CG. Moreover, the CG treatment also significantly alleviated the OA-induced accumulation of prostaglandin (PG) (P < 0.001) and total proteins (P < 0.001) in the synovial fluid. The histopathologic analyses revealed that the CG treatment reduced the severity of the OA-like structural damages in the cartilage. However, the level of PGE2, a pathologic inflammatory molecule, was not diminished by CG or piroxicam. Conclusion: These results indicate that the isoflavonoid CG isolated from AR significantly alleviated the pathologic changes in the OA-like rabbit knee joints. This suggests that CG from AR could be a promising treatment for the therapy of OA. (C) 2007 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.