Abstract
Shexiang-Wulong Pill (SWP) is derived from “Moschus Yuan,” first formulated during the Song Dynasty for the treatment of joint pain. The aim of this study was to evaluate the therapeutic effect of SWP in a mouse model of collagen-induced arthritis (CIA). Forty-five DBA/1 mice were randomly divided into control group, model group, and SWP-treated group. SWP was administered by oral gavage for 22 days after the booster immunization. The clinical arthritic scores and joint histopathology, including synovial hyperplasia and hypoxic regions, cartilage erosion, and bone destruction, were evaluated. Microcomputed tomography (micro-CT) was used to assess microstructural changes in the bone. Serum levels of TNF-a, IL-6, and IFN-γ were measured by enzyme-linked immunosorbent assay (ELISA). The results showed a statistically significant improvement in joint pathological changes in the SWP-treated group. Imaging assessment confirmed that SWP protected the bone tissue from CIA-induced erosion and increased the bone density. In addition, the serum levels of TNF-a, IL-6, and IFN-γ in SWP-treated mice were significantly lower than those in the model group (P<0.05). Taken together, Shexiang-Wulong Pill can effectively alleviate joint swelling in CIA mice, inhibit synovial tissue hyperplasia, reduce inflammatory cell infiltration, and delay bone destruction. These results indicate that Shexiang-Wulong Pills could be an efficient medication for the treatment of RA.
Highlights
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by synoviocyte hyperplasia, inflammatory cell infiltration, synovial pannus formation, and the destruction of cartilage and bone [1]
Arthritic symptoms like joint swelling and loss of appetite were manifested prior to the Collagen Type II (CII) booster, while all mice showed the typical symptoms by Day 30 and peaked on Day 33
collagen-induced arthritis (CIA) mice had body weight loss from Day 28 to Day 42, suggesting that the weight loss in the treatment group may be associated with inflammation
Summary
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by synoviocyte hyperplasia, inflammatory cell infiltration, synovial pannus formation, and the destruction of cartilage and bone [1]. Since the pathogenesis of RA has not been completely elucidated, RA’s therapeutic strategy is concentrated on multiple targets. Conventional drugs such as nonsteroidal antiinflammatory drugs (NSAIDs), corticosteroids, and diseasemodifying antirheumatic drugs (DMARDs) may relieve the symptoms of the disease but are associated with adverse effects like kidney and liver injury, bone loss, and immunosuppression during long-term use. Biological agents such as tumor necrosis factor (TNF) inhibitors are considered to be more effective than former drugs [3]. A systematic review with meta-analysis showed that Tripterygium wilfordii extract monotherapy or combination with DMARDs significantly
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